BISPECIFIC RECOMBINANT PROTEIN AND USE THEREOF

20230365703 · 2023-11-16

    Inventors

    Cpc classification

    International classification

    Abstract

    A bispecific recombinant protein, comprising a first functional binding fragment, a second functional binding fragment, and an Fc region. The first functional binding fragment targeting an antigen of interest of the bispecific recombinant protein comprises an antigen-binding fragment, wherein the C-terminus of the CL domain or the C-terminus of the CH1 domain in the antigen-binding fragment is directly connected to or is connected via a linker to the second functional binding fragment having the functions of immunoregulation and/or metabolic regulation and/or endocrine regulation. The recombinant protein can improve the targeting for the target of the second functional binding fragment of the bispecific recombinant protein and can also reduce toxic side effects caused by the non-target protein containing the second functional binding fragment generated during the preparation process targeting non-target organs, tissues and cells.

    Claims

    1. A bispecific recombinant protein, wherein, the bispecific recombinant protein comprises a first functional binding fragment, a second functional binding fragment, and an Fc region; the first functional binding fragment targeting an antigen of interest of the bispecific recombinant protein comprises an antigen-binding fragment, wherein a C-terminus of a CL domain or a C-terminus of a CH1 domain in the antigen-binding fragment is directly connected to or is connected via a linker to the second functional binding fragment having a function of immunoregulation or a function of metabolic regulation or a function of endocrine regulation; the antigen-binding fragment is directly connected to or is connected via a linker to a N-terminus of the second functional binding fragment, and, a C-terminus of the second functional binding fragment is directly connected to or is connected via a linker to a N-terminus of the Fc region.

    2. The bispecific recombinant protein of claim 1, wherein, the second functional binding fragment having a function of immunoregulation targets an immune checkpoint, an immune checkpoint ligand, or a cytokine receptor; preferably, the second functional binding fragment having a function of immunoregulation targets PD-1 or a ligand thereof, CD47 or a ligand thereof, CD24 or a ligand thereof, an interferon receptor, or an interleukin receptor.

    3. (canceled)

    4. The bispecific recombinant protein of claim 1, wherein, the second functional binding fragment having a function of metabolic regulation targets a metabolic regulator, or a metabolic regulator receptor; preferably, the second functional binding fragment having a function of metabolic regulation targets an insulin receptor, or a fibroblast growth factor receptor.

    5. (canceled)

    6. The bispecific recombinant protein of claim 1, wherein, the second functional binding fragment having a function of endocrine regulation targets an endocrine regulator, or an endocrine regulator receptor; preferably, the second functional binding fragment having a function of endocrine regulation targets a hormone receptor.

    7. (canceled)

    8. The bispecific recombinant protein of claim 1, wherein, a variable region and a constant region in the antigen-binding fragment are directly connected or are connected via a linker; or the antigen-binding fragment and the Fc region are directly connected or are connected via a linker; or both of methods mentioned above are used simultaneously to connect.

    9. The bispecific recombinant protein of claim 1, wherein, the linker sequence comprises (GGGGS)n (SEQ ID NO: 65), (GGGS)n (SEQ ID NO: 66), (GGS)n, (G)n, (GS)n, (EAAAK)n (SEQ ID NO: 67), or (XP)n, n is a natural number; preferably, n is a natural number from 0 to 5.

    10. The bispecific recombinant protein of claim 2, wherein, the second functional binding fragment binds to a cytokine receptor, an immune checkpoint or an immune checkpoint ligand, the second functional binding fragment is cytokine, the immune checkpoint ligand or a binding protein for the immune checkpoint ligand, or a functional fragment thereof or a mutant thereof; the second functional binding fragment is selected from any one of the following: an extracellular functional fragment of human SIRP family, a functional fragment of human interferon family, a functional fragment of tumor necrosis factor superfamily, a functional fragment of TGF-β superfamily, a functional fragment of interleukins, a functional fragment of chemokine family, a functional fragment of colony stimulating factor family, a functional fragment of growth factors, or a mutant thereof; preferably, the second functional binding fragment is an extracellular D1 domain of human SIRPα or a mutant thereof, the second functional binding fragment is a type I or type II human interferon receptor, or the second functional binding fragment is an interleukin, a truncated variant thereof, or a mutant thereof.

    11. (canceled)

    12. The bispecific recombinant protein of claim 10, wherein, the interferon receptor is a human interferon γ (IFN-γ) receptor or a human interferon β (IFN-β) receptor.

    13. (canceled)

    14. The bispecific recombinant protein of claim 10, wherein, the interleukin is an immunoregulatory factor or chemokine selected from any one of the following: IL-1 family, IL-2 family, IL-3 family, IL-6 family, IL-8 family, IL-10 family, IL-12 family, and IL-17 family.

    15. The bispecific recombinant protein of claim 1, wherein, the first functional binding fragment targets any one or more of the following targets: CD20, GPC-3, PD-L1, CD38, EpCAM, CD24, TIGIT, PD-1, CD80, EGFR, AFP, 5T4, AGS-16, ALK1, ANG-2, B7-H3, B7-H4, c-fms, c-Met, CA6, CD123, CD19, CD22, CD30, CD32b, CD37, CD40, CD52, CD70, CD71, CD74, CD79b, CD83, CD86, CD98, CD206, CEA, CEACAM5, CLDN18.2, CLDN6, CS1, CCR5, CXCR4, DLL-4, EGFRvIII, EGP-1, ENPP3, EphA3, ETBR, FGFR2, FN, FR-α, GCC, GD2, GPNMB, HER2, HER3, HLA-DR, ICAM-1, IGF-1R, IL-3R, LIV-1, MSLN, MUC16, MUC1, NaPi2b, Nectin-4, Notch 2, Notch 1, PD-L2, PDGFR-α, PS, PSMA, SLTRK6, STEAP1, TEM1, VEGFR, CD25, CD27L, DKK-1, CSF-1R, MSB0010718C, BCMA, CD138, TROP2, Siglec15, and CD155; preferably, the second functional binding fragment comprises an extracellular D1 domain of human SIRPα or a mutant thereof, a human interferon β or a human interferon γ, or an interleukin, a truncated variant thereof or a mutant thereof, the first functional binding fragment targets a tumor cell or an immune cell.

    16. The bispecific recombinant protein of claim 1, wherein, the bispecific recombinant protein consists of a chain A and a chain B, the chain A binds to the chain B by intermolecular force, by covalent bond, or by salt bond, or by a combination of two or three of binding methods mentioned above; preferably, the Fc region comprises an Fc region native sequence or an Fc region non-native sequence; more preferably, the Fc region is a human Fc region; further more preferably, the Fc region of the chain A binds to the Fc region of the chain B by knobs-into-holes; or, the Fc region is an Fc region of human IgG; even more preferably, the Fc region is an Fc region of human IgG1 or IgG4.

    17. (canceled)

    18. (canceled)

    19. The bispecific recombinant protein of claim 16, wherein, the C-terminus of the CL domain, the C-terminus of the CH1 domain or the C-terminus of the second functional binding fragment is directly connected to the Fc region or is connected via a linker to the Fc region.

    20. The bispecific recombinant protein of claim 16, wherein, the first functional binding fragment is any one or more of antigen-binding fragments targeting the following targets: CD20, GPC-3, PD-L1, CD38, EpCAM, CD24, TIGIT, PD-1, CD80, EGFR, AFP, 5T4, AGS-16, ALK1, ANG-2, B7-H3, B7-H4, c-fms, c-Met, CA6, CD123, CD19, CD22, CD30, CD32b, CD37, CD40, CD52, CD70, CD71, CD74, CD79b, CD83, CD86, CD98, CD206, CEA, CEACAM5, CLDN18.2, CLDN6, CS1, CCR5, CXCR4, DLL-4, EGFRvIII, EGP-1, ENPP3, EphA3, ETBR, FGFR2, FN, FR-α, GCC, GD2, GPNMB, HER2, HER3, HLA-DR, ICAM-1, IGF-1R, IL-3R, LIV-1, MSLN, MUC16, MUC1, NaPi2b, Nectin-4, Notch 2, Notch 1, PD-L2, PDGFR-α, PS, PSMA, SLTRK6, STEAP1, TEM1, VEGFR, CD25, CD27L, DKK-1, CSF-1R, MSB0010718C, BCMA, CD138, TROP2, Siglec15, and CD155; the antigen-binding fragment is a human-mouse chimeric antigen-binding fragment, a humanized antigen-binding fragment, or a fully human antigen-binding fragment.

    21. The bispecific recombinant protein of claim 20, wherein, when the first functional binding fragment targets CD20, EGFR, EGFRvIII, PD-L1, PD-L2, HER2, HER3, CD138, CD44, CD24, EpCAM, CLDN18.2, CD38, BCMA, MUC1, or TROP2, the second functional binding fragment comprises an extracellular D1 domain of SIRPα or a mutant thereof; when the first functional binding fragment targets TIGIT, Siglec15, PD-1, PD-L1, PD-L2, CD71, CD80, CD86, CD206, or CCR5, the second functional binding fragment comprises IFN-β, IFN-γ, IL-10M, IL-12A, or a complex formed by IL-15 and IL15RαSUSHI, or a mutant thereof; preferably: the first functional binding fragment targets CD20, EpCAM, CD24, or EGFR, the second functional binding fragment comprises an extracellular D1 domain of SIRPα or a mutant thereof; preferably, amino acid sequence of the second functional binding fragment is as shown in SEQ ID NO: 50; more preferably, amino acid sequence of the chain A is as shown in SEQ ID NO: 1, amino acid sequence of the chain B is as shown in SEQ ID NO: 2 or 3; amino acid sequence of the chain A is as shown in SEQ ID NO: 61, amino acid sequence of the chain B is as shown in SEQ ID NO: 62; amino acid sequence of the chain A is as shown in SEQ ID NO: 27, amino acid sequence of the chain B is as shown in SEQ ID NO: 28; amino acid sequence of the chain A is as shown in SEQ ID NO: 29, amino acid sequence of the chain B is as shown in SEQ ID NO: 30; amino acid sequence of the chain A is as shown in SEQ ID NO: 56, amino acid sequence of the chain B is shown in SEQ ID NO: 57; the first functional binding fragment targets TIGIT, CD80 or PD-1, the second functional binding fragment comprises IL-12A, an IL-10 monomer mutant, or a complex formed by 1L15 and IL-15RαSUSHI, amino acid sequences of the IL-12A, IL-10 monomer mutant, and IL15 and IL-15RαSUSHI are as shown in SEQ ID NOs: 51, 52, 53, and 54, respectively, or a mutant of the second functional binding fragment mentioned above; preferably, amino acid sequence of the chain A is as shown in SEQ ID NO:35, amino acid sequence of the chain B is as shown in SEQ ID NO:36; amino acid sequence of the chain A is as shown in SEQ ID NO:37, amino acid sequence of the chain B is as shown in SEQ ID NO: 38; amino acid sequence of the chain A is as shown in SEQ ID NO: 39, amino acid sequence of the chain B is as shown in SEQ ID NO: 40 or 41; the first functional binding fragment targets CD38 or AFP, the second functional binding fragment comprises an extracellular D1 domain of SIRPα or a mutant thereof, or IFN-β or a mutant thereof; preferably, amino acid sequence of the second functional binding fragment is as shown in SEQ ID NO: 50 or 55; more preferably, amino acid sequence of the chain A is as shown in SEQ ID NO: 31, amino acid sequence of the chain B is as shown in SEQ ID NO: 32; amino acid sequence of the chain A is as shown in SEQ ID NO: 33, amino acid sequence of the chain B is as shown in SEQ ID NO: 34; or, amino acid sequence of the chain A is as shown in SEQ ID NO: 58, amino acid sequence of the chain B is as shown in SEQ ID NO: 60.

    22. A nucleic acid molecule encoding the bispecific recombinant protein of claim 1; wherein, a nucleic acid molecule encoding the first functional binding fragment and a nucleic acid encoding the second functional binding fragment are in a same DNA strand, or a nucleic acid molecule encoding the first functional binding fragment and a nucleic acid encoding the second functional binding fragment are in different DNA strands; preferably, a nucleic acid molecule encoding the Fc region is in a same DNA strand with the nucleic acid encoding the first functional binding fragment or the second functional binding fragment, a nucleic acid molecule encoding the Fc region is in different DNA strands with the nucleic acid encoding the first functional binding fragment or the second functional binding fragment.

    23. An expression vector comprising the nucleic acid molecule of claim 22.

    24. A host cell transformed with the expression vector of claim 23.

    25. A method for preparing the bispecific recombinant protein of claim 24, the host cell is cultured under a condition suitable for expression, and then the bispecific recombinant protein is obtained by expression.

    26. A medicament or pharmaceutical composition, wherein, the medicament or pharmaceutical composition comprises the bispecific recombinant protein of claim 1.

    27. A method for treating tumors, autoimmune diseases, infectious diseases, sepsis, graft-versus-host diseases, metabolic disorders, endocrine disorders comprising administrating an effective amount of the bispecific recombinant protein of claim 1 to a subject in need of; preferably, the tumor is a solid tumor or a hematological tumor; preferably, the solid tumor is selected from any one of the following: breast cancer, colorectal cancer, lung cancer, pancreatic cancer, esophagus cancer, endometrial cancer, ovarian cancer, gastric cancer, prostate cancer, renal cancer, cervical cancer, thyroid cancer, uterine cancer, bladder cancer, neuroendocrine cancer, head and neck cancer, liver cancer, nasopharyngeal cancer, testicular cancer, small cell lung cancer, non-small cell lung cancer, melanoma, basal cell carcinoma, squamous cell carcinoma, dermatofibrosarcoma protuberan, Merkel cell carcinoma, glioblastoma, glioma, sarcoma, mesothelioma, and myelodysplastic syndrome; the hematological tumor is selected from myeloma, lymphoma or leukemia; the autoimmune disease is selected from any one of the following: Hashimoto's thyroiditis, type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, and sjogren syndrome; the infectious disease is selected from any one of the following: viral infections, bacterial infections, fungal infections, and other pathogenic infections.

    28. (canceled)

    Description

    BRIEF DESCRIPTION OF THE DRAWINGS

    [0141] FIG. 1 shows a structural diagram of the bispecific recombinant protein of the present disclosure.

    [0142] FIG. 2 shows SDS-PAGE electrophoresis diagrams of the bispecific recombinant protein in Embodiment 2 of the present disclosure after purification by protein A.

    [0143] FIG. 3 shows non-reducing SDS-PAGE electrophoresis diagrams of the bispecific recombinant protein in Embodiment 2 of the present disclosure after affinity capture.

    [0144] FIG. 4 shows a reducing SDS-PAGE electrophoresis diagrams of the bispecific recombinant protein in Embodiment 2 of the present disclosure after affinity capture.

    [0145] FIG. 5 shows non-reducing SDS-PAGE electrophoresis diagrams of the bispecific recombinant protein in Embodiment 2 of the present disclosure after secondary purification.

    [0146] FIG. 6 shows a binding curve of the bispecific recombinant protein of the present disclosure to CD20 single-positive cells (non-target cells of interest, CHO-K1-hCD20) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0147] FIG. 7A shows a binding curve of the bispecific recombinant protein whose second functional antigen is CD47 of the present disclosure and the control sample to CD47 single-positive cells (non-target cells of interest, HEK293 cells) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0148] FIG. 7B shows a binding curve of the bispecific recombinant protein whose second functional antigen is CD47 of the present disclosure and the control sample to CD47 single-positive cells (non-target cells of interest, CHO-K1 cells) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0149] FIG. 8 shows a binding curve of the bispecific recombinant protein whose first functional antigen is CD20 and whose second functional antigen is CD47 of the present disclosure and the control sample to CD20/CD47 double-positive cells (target cells of interest, Raji cells) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0150] FIG. 9A shows a competitive binding curve of the bispecific recombinant protein whose first functional antigen is CD20 and whose second functional antigen is CD47 of the present disclosure, the corresponding potentially risky impurity protein, and the control sample to CD20/CD47 double-positive cells (target cells of interest, Raji cells) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0151] FIG. 9B shows a competitive binding curve of the bispecific recombinant protein whose first functional antigen is EpCAM and whose second functional antigen is CD47 of the present disclosure and the control sample to EpCAM/CD47 double-positive cells (target cells of interest, CAPAN-2 cells) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0152] FIG. 9C shows a competitive binding curve of the bispecific recombinant protein whose first functional antigen is CD24 and whose second functional antigen is CD47 of the present disclosure and the control sample to CD24/CD47 double-positive cells (target cells of interest, MCF-7 cells) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0153] FIG. 9D shows a competitive binding curve of the bispecific recombinant protein whose first functional antigen is CD38 and whose second functional antigen is CD47 of the present disclosure and the control sample to CD38/CD47 double-positive cells (target cells of interest, Raji cells) determined by flow cytometry in Embodiment 3 of the present disclosure.

    [0154] FIG. 10 shows a binding activity curve of the bispecific recombinant protein whose first functional antigen is GPC3 and whose second functional antigen is IFN-α 2b in Embodiment 4 of the present disclosure and the control sample to target cells of interest, HepG2 hepatoma cells, determined by flow cytometry.

    [0155] FIG. 11 shows a binding activity histogram of the bispecific recombinant protein whose first functional antigen is GPC3 and whose second functional antigen is IFN-α 2b in Embodiment 4 of the present disclosure and the control sample to target cells of interest HuH-7 determined by flow cytometry.

    [0156] FIG. 12 shows an ADCC activity curve of the bispecific recombinant protein in Embodiment 5 of the present disclosure to target cells of interest HepG2 determined by LDH method.

    [0157] FIG. 13 shows a proliferation inhibition activity curve of the bispecific recombinant protein with different linkers in Embodiment 6 of the present disclosure to target cells of interest HUH-7.

    [0158] FIG. 14 shows a proliferation inhibition activity curve of the bispecific recombinant protein having the GPC3 antigen targeting function in Embodiment 6 of the present disclosure and the control sample to GPC3-positive target cells of interest HuH-7.

    [0159] FIG. 15 shows a proliferation inhibition activity curve of the bispecific recombinant protein in Embodiment 7 of the present disclosure to PD-L1-positive target cells of interest MDA-MB-231.

    [0160] FIG. 16 shows a proliferation inhibition activity curve of the bispecific recombinant protein in Embodiment 7 of the present disclosure to MDA-MB-231 blocked with anti-PD-L1 antibody.

    [0161] FIG. 17A shows a proliferation inhibition activity curve of the bispecific recombinant protein in Embodiment 8 of the present disclosure to CD38-positive target cells of interest Daudi.

    [0162] FIG. 17B shows a proliferation inhibition activity curve of the bispecific recombinant protein in Embodiment 8 of the present disclosure to CD38-negative non-target cells of interest SK-BR3.

    [0163] FIG. 18 shows a proliferation inhibition activity curve of the bispecific recombinant protein containing different IFN-α 2b low-affinity mutants in Embodiment 9 of the present disclosure to GPC3-positive target cells of interest HuH-7.

    [0164] FIG. 19 shows a proliferation inhibition activity curve of the bispecific recombinant protein containing different IFN-α 2b low-affinity mutants in Embodiment 9 of the present disclosure to GPC3-negative non-target cells of interest SW480.

    [0165] FIG. 20 shows a proliferation inhibition activity curve of the bispecific recombinant protein containing different IFN-α 2b low-affinity mutants in Embodiment 9 of the present disclosure to GPC3-negative non-target cells of interest U266.

    [0166] FIG. 21 shows a proliferation inhibition activity curve of the potentially risky impurities of the bispecific recombinant protein in Embodiment 10 of the present disclosure to GPC3-negative non-target cells of interest MDA-MB-231.

    [0167] FIG. 22 shows a binding activity curve of the bispecific recombinant protein in Embodiment 11 of the present disclosure to TIGIT-positive target cells of interest H_IL12 Reporter 293 blocked with anti-TIGIT antibody.

    [0168] FIG. 23 shows P-STAT3 activation level assay results of the bispecific recombinant protein in Embodiment 12 of the present disclosure to THP1 cells.

    [0169] FIG. 24 shows proliferation activity assay results of the bispecific recombinant protein in Embodiment 13 of the present disclosure to PD-1-positive hPBMC stimulated with OKT3 for 48 hours.

    [0170] FIG. 25 shows proliferation activity assay results of the bispecific recombinant protein in Embodiment 13 of the present disclosure to PD-1-negative non-target cells of interest M-07e.

    DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENT

    Embodiment 1: Construction of Expression Vector

    [0171] The bispecific recombinant protein was directly synthesized by GENEWIZ after codon optimization according to the protein sequence, and was inserted into the pCDNA3.1 plasmid, which was confirmed by sequencing. The above-mentioned different expression plasmids were mixed and paired to transfect expressing cells to obtain bispecific recombinant proteins or control samples (see Table 1). Subsequent experimental materials were extracted and obtained from expressing cells transfected with this series of plasmids.

    TABLE-US-00001 TABLE 1 Exemplary molecular structures of bispecific recombinant proteins and control samples Bispecific recombinant protein Number of First functional bispecific antigen × second recombinant functional Exemplary bi-clonal antibody molecular constitution protein binding fragment chain A chain B LCB-001 CD20 × SIRPαD1 Ofatumumab(H)-Fc1 Ofatumumab(L)-SIRPαD1- Fc2 LCB-002 CD20 × SIRPαD1 Ofatumumab(H)-Fc1 Ofatumumab(L)-(GGGGS).sub.3- SIRPαD1-Fc2 LCB-003 CD20 × SIRPαD1 Ofatumumab(H)-(GGGS)3- Ofatumumab(L)-Fc2 SIRPαD1-Fc1 LCB-004 EGFR × SIRPαD1 Panitumumab(H)-Fc1 Panitumumab(L)- (GGGGS).sub.3-SIRPαD1-Fc2 LCB-005 EpCAM × SIRPαD1 Edrecolomab (H)-Fc1 Edrecolomab (L)- (GGGGS).sub.5-SIRPαD1-Fc2 LCB-006 CD24 × SIRPαD1 SWA11(H)-Fc1 SWA11(L)-(GGGGS).sub.2- SIRPαD1-Fc2 LCB-007 AFP × IFNα 2b Tacatuzumab(H)-Fc1 Tacatuzumab(L)-(GGGGS).sub.3- IFNα 2b-Fc2 LCB-008 AFP × IFNβ Tacatuzumab(H)-Fc1 Tacatuzumab(L)-(GGGGS).sub.3- IFNβ-Fc2 LCB-009 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.1-IFNα 2b-Fc2 LCB-010 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.2-IFNα 2b-Fc2 LCB-011 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.4-IFNα 2b-Fc2 LCB-010-M1 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.2-IFNα 2b(L26A)-Fc2 LCB-010-M2 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.2-IFNα 2b(L30A)-Fc2 LCB-010-M3 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.2-IFNα 2b(A145G)-Fc2 LCB-010-M4 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.2-IFNα 2b(R149A)-Fc2 LCB-010-M5 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.2-IFNα 2b(S152A)-Fc2 LCB-011-M3 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.4- IFNα 2b(A145G)-Fc2 LCB-011-M4 GPC3 × IFN-α 2b GC33(H)-Fc1 GC33(L)-(GGGGS).sub.4-IFNα 2b(R149A)-Fc2 LCB-012 RSV × IFN-α 2b Palivizumab(H)- Fc1 Palivizumab (L)-(GGGGS).sub.2- IFNα 2b -Fc2 LCB-013 PD-L1 × IFN-α 2b Atezolizumab (H)-Fc1 Atezolizumab (L)- (GGGGS).sub.1-IFNα 2b-Fc2 LCB-014 PD-L1 × IFN-α 2b Atezolizumab (H)-Fc1 Atezolizumab (L)- (GGGGS).sub.2-IFNα 2b-Fc2 LCB-015 PD-L1 × IFN-α 2b Atezolizumab (H)-Fc1 Atezolizumab (L)- (GGGGS).sub.3-IFNα 2b-Fc2 LCB-016 CD38 × IFN-α 2b Mezagitamab(L)-Fc1 Mezagitamab (H)- (GGGGS).sub.5-IFNα2b-Fc2 LCB-017 CD38 × SIRPαD1 Felzartamab(H)-Fc2 Felzartamab(L)-(GGGGS).sub.5- SIRPαD1-Fc1 LCB-018 TIGIT × IL-12 Tiragolumab(H)-Fc1 Tiragolumab (L)-(GGGGS).sub.4- IL12A-Fc2 LCB-019 CD80 × IL-10 Galiximab(H)-Fc1 Galiximab(L)- (GGGGS).sub.5- IL10M-Fc2 LCB-020 PD-1 × IL-15- Nivolumab(H)-Fc1 Nivolumab(L)-(GGGGS).sub.5- IL15RαSUSHI IL15-(GGGGS).sub.5- IL15RαSUSHI-Fc2 LCB-021 PD-1 × IL-15- Nivolumab(H)-Fc1 Nivolumab(L)-(GGGGS).sub.5- IL15RαSUSHI IL15RαSUSHI-(GGGGS).sub.5- IL15-Fc2 LCB-022 RSV × IL-10 Palivizumab(H)- Fc1 Palivizumab (L)- (GGGGS).sub.5-IL10M-Fc2 LCB-023 RSV × IL-15- Palivizumab(H)- Fc1 Palivizumab (L)-(GGGGS).sub.5- IL15RαSUSHI IL15-(GGGGS).sub.5- IL15RαSUSHI-Fc2 LCB-024 RSV × IL-15- Palivizumab(H)- Fc1 Palivizumab (L)-(GGGGS).sub.5- IL15RαSUSHI IL15RαSUSHI-(GGGGS).sub.5- IL15-Fc2 Control sample Name of control sample Antigen Molecular constitution Ofatumumab CD20 Anti-CD20 monoclonal antibody Ofatumumab Rituximab CD20 Anti-CD20 monoclonal antibody Rituximab Magrolimab CD47 Anti-CD47 monoclonal antibody Magrolimab Ofa-Fc1-D1-Fc2 CD20 × CD47 Ofatumumab-Fc1, D1-Fc2 (see CN108864290A SEQ ID NO: 16 (Ofa-Fc1 heavy chain) + SEQ ID NO: 17 (Ofa-Fc1 light chain) + SEQ ID NO: 26 (D1-Fc2)) TTI-621 CD47 SIRPαD1-Fc homodimer (see CN105073780B SEQ ID NO: 25) SIRPα-D1m-Fc CD47 SIRPαD1m-Fc homodimer (D1m sequence, see CN108864290A SEQ ID NO: 33) LCB-001-R CD47 Ofatumumab(L)-SIRPαD1-Fc2 homodimer LCB-002-R CD47 Ofatumumab(L)-(GGGGS).sub.3-SIRPαD1-Fc2 homodimer Codrituzum ab GPC3 Anti-GPC3 monoclonal antibody codrituzumab Palivizumab Respiratory Anti-RSV monoclonal antibody Palivizumab syncytial virus (RSV) Atezolizumab PD-L1 Anti-PD-L1 monoclonal antibody Atezolizumab Felzartamab CD38 Anti-CD38 monoclonal antibody Felzartamab Mezagitamab CD38 Anti-CD38 monoclonal antibody Mezagitamab Tiragolumab TIGIT Anti-TIGIT monoclonal antibody Tiragolumab Galiximab CD80 Anti-CD80 monoclonal antibody Galiximab Nivolumab PD-1 Anti-PD-1 monoclonal antibody Nivolumab IFN-α 2b-Fc None Recombinant expression of IFN-α 2b and human IgG1 Fc fusion protein IFN-α 2b None Recombinant expression of IFN-α 2b protein IL10M-Fc None Recombinant expression of human IL10 monomer mutant and human IgG1 Fc fusion protein IL15- None Recombinant expression of human IL15, IL15RαSUSHI IL15RαSUSHI-Fc and human IgG1 Fc fusion protein Human IgG1 Hen egg Anti-HEL monoclonal antibody as homotype control homotype control lysozyme (HEL) (Isotype)

    [0172] In the Table 1 above, the first functional binding fragment of the bispecific recombinant protein is characterized by the antigen of interest it targets, namely the first functional antigen; (H) refers to the domain consisting of heavy chains VH and CHL (L) refers to the domain consisting of light chains VL and CL; D1 represents the extracellular D1 domain of wild-type human SIRPα and its mutants; Fc represents the wild-type Fc region, Fc1 represents the Fc region with hole or holes mutation, and Fc2 represents the Fc region with knob or knobs mutation. The corresponding sequence numbers of the sequence names are shown in Table 2. Herein, the sequence of the signal peptide is shown in SEQ ID NO: 49. The amino acid sequence of Codrituzumab is referenced from the U.S. Pat. No. 7,919,086, the amino acid sequence of the heavy chain is shown in SEQ ID NO: 19, and the amino acid sequence of the light chain is shown in SEQ ID NO: 20. The amino acid sequence of Atezolizumab is referenced from the patent US20100203056, the amino acid sequence of the heavy chain is shown in SEQ ID NO: 21, and the amino acid sequence of the light chain is shown in SEQ ID NO: 22. The amino acid sequence of the heavy chain of Tiragolumab is shown in SEQ ID NO: 61, and the amino acid sequence of the light chain is shown in SEQ ID NO: 62. The amino acid sequences of heavy chain variable region and light chain variable region of Palivizumab are referenced from the patent WO1994017105. Human IgG1 isotype control (B117901) was purchased from Biointron. Recombinantly expressed IFN-α 2b protein (Z03003) was purchased from Nanjing GenScript Biotechnology Co., Ltd. IL10 in IL10M-Fc was in the form of a monomer mutant, and the corresponding sequence is referred from the following reference (Josephson, K. Design and analysis of an engineered human interleukin-10 monomer. [J]. Journal of Biological Chemistry, 2000, 275 (18): 13552-7.). IL15-IL15RαSUSHI-Fc (C15Y) was purchased from Novoprotein.

    TABLE-US-00002 TABLE 2 Sequence name and corresponding sequence number Sequence name Sequence number Ofatumumab(H)-Fc1 SEQ ID NO: 1 Ofatumumab(L)-SIRPαD1-Fc2 SEQ ID NO: 2 Ofatumumab(L)-(GGGGS).sub.3-SIRPαD1-Fc2 SEQ ID NO: 3 GC33(H)-Fc1 SEQ ID NO: 4 GC33(L)-(GGGGS).sub.1-IFNα 2b-Fc2 SEQ ID NO: 5 GC33(L)-(GGGGS).sub.2-IFNα 2b-Fc2 SEQ ID NO: 6 GC33(L)-(GGGGS).sub.4-IFNα 2b-Fc2 SEQ ID NO: 7 GC33(L)-(GGGGS).sub.2-IFNα 2b(L26A)-Fc2 SEQ ID NO: 8 GC33(L)-(GGGGS).sub.2-IFNα 2b(L30A)-Fc2 SEQ ID NO: 9 GC33(L)-(GGGGS).sub.2-IFNα 2b(A145G)-Fc2 SEQ ID NO: 10 GC33(L)-(GGGGS).sub.2-IFNα 2b(R149A)-Fc2 SEQ ID NO: 11 GC33(L)-(GGGGS).sub.2-IFNα 2b(S152A)-Fc2 SEQ ID NO: 12 GC33(L)-(GGGGS).sub.4-IFNα 2b(A145G)-Fc2 SEQ ID NO: 13 GC33(L)-(GGGGS).sub.4-IFNα 2b(R149A)-Fc2 SEQ ID NO: 14 Palivizumab(H)- Fc1 SEQ ID NO: 15 Palivizumab (L)-(GGGGS).sub.2-IFNα 2b-Fc2 SEQ ID NO: 16 IFN-α 2b-Fc1 SEQ ID NO: 17 IFN-α 2b SEQ ID NO: 18 GC33(H)-Fc SEQ ID NO: 19 GC33(L) SEQ ID NO: 20 Atezolizumab(H)-Fc SEQ ID NO: 21 Atezolizumab(L) SEQ ID NO: 22 Atezolizumab (H)-Fc1 SEQ ID NO: 23 Atezolizumab (L)-(GGGGS).sub.1-IFNα 2b-Fc2 SEQ ID NO: 24 Atezolizumab (L)-(GGGGS).sub.2-IFNα 2b-Fc2 SEQ ID NO: 25 Atezolizumab (L)-(GGGGS).sub.3-IFNα 2b-Fc2 SEQ ID NO: 26 Edrecolomab (H)-Fc1 SEQ ID NO: 27 Edrecolomab (L)-(GGGGS).sub.5- SIRPαD1-Fc2 SEQ ID NO: 28 SWA11(H)-Fc1 SEQ ID NO: 29 SWA11(L)-(GGGGS).sub.2- SIRPαD1-Fc2 SEQ ID NO: 30 Mezagitamab(L)-Fc1 SEQ ID NO: 31 Mezagitamab (H)-(GGGGS).sub.5-IFNα2b-Fc2 SEQ ID NO: 32 Felzartamab(H)-Fc2 SEQ ID NO: 33 Felzartamab(L)-(GGGGS).sub.5- SIRPαD1-Fc1 SEQ ID NO: 34 Tiragolumab(H)-Fc1 SEQ ID NO: 35 Tiragolumab (L)-(GGGGS).sub.4-IL12A-Fc2 SEQ ID NO: 36 Galiximab(H)-Fc1 SEQ ID NO: 37 Galiximab(L)- (GGGGS).sub.5-IL10M-Fc2 SEQ ID NO: 38 Nivolumab(H)-Fc1 SEQ ID NO: 39 Nivolumab(L)-(GGGGS).sub.5-IL15-(GGGGS).sub.5-IL15RαSUSHI-Fc2 SEQ ID NO: 40 Nivolumab(L)-(GGGGS).sub.5-IL15RαSUSHI-(GGGGS).sub.5-IL15-Fc2 SEQ ID NO: 41 Palivizumab (L)-(GGGGS).sub.5-IL10M-Fc2 SEQ ID NO: 42 Palivizumab(L)-(GGGGS).sub.5-IL15-(GGGGS).sub.5- IL15RαSUSHI-Fc2 SEQ ID NO: 43 Palivizumab (L)-(GGGGS).sub.5-IL15RαSUSHI-(GGGGS).sub.5-IL15-Fc2 SEQ ID NO: 44 Felzartamab(H)-Fc SEQ ID NO: 45 Felzartamab(L) SEQ ID NO: 46 IL10M-Fc SEQ ID NO: 47 IL12B SEQ ID NO: 48 Signal peptide SEQ ID NO: 49 SIRPαD1 SEQ ID NO: 50 IL-12A SEQ ID NO: 51 IL-10M SEQ ID NO: 52 IL-15 SEQ ID NO: 53 IL-15RαSUSHI SEQ ID NO: 54 IFN ß SEQ ID NO: 55 Panitumumab (H)-Fc1 SEQ ID NO: 56 Panitumumab(L)-(GGGGS).sub.3-SIRPαD1-Fc2 SEQ ID NO: 57 Tacatuzumab(H)-Fc1 SEQ ID NO: 58 Tacatuzumab(L)-(GGGGS).sub.3-IFNα 2b-Fc2 SEQ ID NO: 59 Tacatuzumab(L)-(GGGGS).sub.3-IFN ß-Fc2 SEQ ID NO: 60 Ofatumumab(H)-(GGGS).sub.3-SIRPαD1-Fc1 SEQ ID NO: 61 Ofatumumab(L)-Fc2 SEQ ID NO: 62 Tiragolumab(H)-Fc SEQ ID NO: 63 Tiragolumab (L) SEQ ID NO: 64

    [0173] In Table 1, human IFN-α 2b (Genebank: AAP20099.1) was used as an example to illustrate the design of IFNα as a second functional binding fragment of the bispecific recombinant protein. There are 15 subtypes in the IFNα family. Different subtypes have similar structures, high sequence homology (80-99%), and bind to the same IFN receptors. All subtypes have the functions of antivirus, proliferation inhibition, antitumor and immunoregulation. Regarding the technical effects that can be achieved by IFN-α 2b, the other subtypes of IFN-α can achieve the identical technical effects (British Journal of Pharmacology (2013) 168 1048-1058), which will not be repeated here in the present disclosure. IFN-β and IFN-α 2b have the same interferon receptor and are both type I interferons and have similar biological effects, therefore they can also achieve the identical technical effects.

    [0174] The structure of the bispecific recombinant protein of the present disclosure is shown in FIG. 1, the first functional binding fragment targeting the antigen of interest of the bispecific recombinant protein comprises an antigen-binding fragment, wherein the C-terminus of the CL domain and the C-terminus of the CH1 domain in the antigen-binding fragment is directly connected to or is connected via a linker to the second functional binding fragment targeting the immune checkpoint or the immune checkpoint ligand or the cytokine receptor. The variable region (V region) and the constant region (C region) in the antigen-binding fragment of the first functional binding fragment are directly connected or are connected via a linker; or the antigen-binding fragment is directly connected to or is connected via a linker to the Fc region; or both above-mentioned methods are used simultaneously to connect. The light chain VL or heavy chain VH of the first functional binding fragment is bound to the second functional binding fragment via knobs-into-holes. The light chain VL or heavy chain VH of the first functional binding fragment or the second functional binding fragment is directly connected to or is connected via a linker to the Fc region. For example, in FIG. 1, a and e represent that the C-terminus of the CL domain of the antigen-binding fragment of the first functional binding fragment is directly connected to or is connected via a linker to the second functional binding fragment; b and f represent that the C-terminus of the CH1 domain of the antigen-binding fragment of the first functional binding fragment is directly connected to or is connected via a linker to the second functional binding fragment; c, g, j, and k represent that the C-terminus of the CL domain of the antigen-binding fragment of the first functional binding fragment is directly connected to or is connected via a linker to the second functional binding fragment, and the Fc region is bound via knobs-into-holes; d, h, i, and l represent that the C-terminus of the CH1 domain of the antigen-binding fragment of the first functional binding fragment is directly connected to or is connected via a linker to the second functional binding fragment, and the Fc region is bound via knobs-into-holes.

    Embodiment 2: Preparation of Expression Plasmid, Cell Transfection, and Expression and Purification of Target Protein

    [0175] 1. Preparation of Expression Plasmid

    [0176] A bacterial glycerol stock containing the expression plasmid (1 mL of the E. coli bacterial solution containing the expression plasmid was added with 0.5 mL of 60% sterile glycerol solution and mixed thoroughly) was inoculated into a liquid LB medium at a ratio of 1:1000. The bacteria were collected by centrifugation at 37° C., 220 rpm after culturing in a shaker for 16 hours. An endotoxin-free plasmid maxiprep kit (DP117, purchased from Tiangen Biotech (Beijing) Co., Ltd.) was used to extract the expression plasmid according to the standard procedure provided by the kit instruction.

    [0177] 2. Cell Transfection and Protein Expression

    [0178] The following method takes LCB-001 as an example, and is suitable for the bispecific recombinant protein whose second functional antigen is CD47.

    [0179] After the obtained expression plasmid was filtered with a 0.22 μm filter membrane, 3 mg of the plasmid (wherein the ratio of expression plasmids of the chain A and chain B of the bispecific recombinant protein was 1:1 (molar ratio)) was added to 50 mL of Opti MEM I Reduced Serum Medium (GIBCO) and mixed thoroughly. 6 mg of transfection reagent polyetherimide (PEI, purchased from Polysciences, dissolved in sterile ultrapure water at a concentration of 1 mg/mL) was pipetted into 50 mL of Opti MEM I Reduced Serum Medium and mixed thoroughly. The obtained PEI solution was added to the Opti MEM I Reduced Serum Medium solution containing the plasmid and mixed thoroughly. After standing at room temperature for 15 minutes, the mixture of plasmid and PEI was slowly and evenly added to a suspension of host cell CHO-S (Thermo Fisher) with a volume of 1 L and a cell density of 3×10.sup.6 cells/mL, and cultured in a 37° C., 5% CO.sub.2 incubator. After 4 hours, a feed medium (the formulation of the feed medium was 80 g of CD Efficient FeedC AGT (Gibco) and 75 g of 5×00483 (Kerry) dissolved in 1L of water) with a volume equivalent to 7% of the initial volume was added therein. The culture temperature was reduced to 33° C. and the cells were harvested after 6 days of culture. The cell suspension was centrifuged at 10° C., 10,000 g for 30 minutes, and the supernatant obtained by centrifugation, i.e., the cell culture harvest solution, was used for purification of the target protein.

    [0180] The following method takes LCB-009 as an example, and is suitable for the bispecific recombinant protein whose second functional antigen is other than CD47.

    [0181] After the obtained expression plasmid was filtered with a 0.22 μm filter membrane, 50 μg of the plasmid (wherein the mass ratio of expression plasmids of the chain A and chain B was 2:1 or 3:1) was added to 2 mL of OptiPRO SFM Medium (GIBCO) and mixed thoroughly. 160 μL of transfection reagent ExpiFectamine CHO Reagent was pipetted into 2 mL of OptiPRO SFM Medium and mixed thoroughly. The obtained mixed solution of transfection reagent was added to the mixed solution containing plasmid and mixed thoroughly. The mixture of plasmid and transfection reagent was slowly and evenly added to a suspension of host cell ExpiCHO-S (Thermo Fisher) with a volume of 50 mL and a cell density of 6×10.sup.6 viable cells/mL, and cultured in a 37° C., 8% CO.sub.2 incubator. On day 1 (after 18-22 hours), 300 μL of ExpiCHO Enhancer and 8 mL of ExpiCHO Feed were added, and the culture temperature was reduced to 32° C.; on day 5, a second feed was performed, supplemented with 8 mL of ExpiCHO Feed, and the cells were harvested after 12 days. The cell suspension was centrifuged at 8000 rpm for 15 minutes, and the supernatant obtained by centrifugation, i.e., the cell culture harvest solution, was used for purification of the target protein.

    [0182] 3. Protein Purification

    [0183] 1) Sample Capture (Protein A Affinity Capture)

    [0184] The following method takes LCB-001 as an example, and is suitable for all bispecific recombinant proteins of the present disclosure.

    [0185] The above-mentioned cell culture harvest solution of LCB-001 was centrifuged at 10,000 rpm for 30 minutes to remove the cells and fragments thereof, then loaded onto a Protein A affinity column (GE Healthcare), and eluted to harvest the target protein. The purity of the protein was detected by SDS-PAGE.

    [0186] The purification method of Protein A is a conventional protein purification method well known to those skilled in the art, the detailed method can be found in the GE Healthcare Protein A product instructions and GE Antibody Purification Manual.

    [0187] 2) Sample Secondary Purification

    [0188] The following method takes LCB-009 as an example to illustrate the secondary purification steps of the bispecific recombinant protein, and is suitable for the bispecific recombinant protein containing many more aggregations after Protein A affinity capture.

    [0189] SULFATE 650F packing (TOSOH) was used to remove the aggregations and other impurities in the sample of the expression supernatant of bispecific recombinant protein LCB-009. The experimental procedures are as follows: [0190] a) equilibration: an equilibration solution (50 mM NaAC-HAC, pH5.5) was used to equilibrate the column until the UV detection line is stable; [0191] b) loading: the sample was loaded by the sample pump, the retention time was 5 min, and the loading capacity was <50 mg/mL; [0192] c) re-equilibration: the equilibration solution (50 mM NaAC-HAC, pH5.5) was used to wash the chromatography column for 5 column volumes; [0193] d) elution: an eluent (50 mM NaAC-HAC, 250 Mm, pH 5.5) was used to elute the target protein, and SDS-PAGE was used to detect the purity of the protein.

    [0194] The purification steps of the control sample in Table 1 were obtained with reference to the operation steps of 1) Sample capture (Protein A affinity capture).

    [0195] The SDS-PAGE protein electrophoresis assay results of the purified bispecific recombinant protein, the control sample and the potentially risky impurities are shown in FIG. 2-FIG. 5.

    [0196] The theoretical molecular weights of the four proteins, LCB-001, LCB-002, LCB-001-R and LCB-002-R, are 111 kD, 114 kD, 123 kD and 129 kD, respectively. As shown in FIG. 2, the target proteins in each lane are normally expressed, but different degrees of left arm dimer, right arm dimer (LCB-001-R, LCB-002-R) and/or multimer are observed in LCB-001 and LCB-002 (lane 1 and lane 2 in FIG. 2).

    [0197] The theoretical molecular weights of LCB-009, LCB-010, LCB-011, LCB-012, LCB-013, LCB-014, LCB-015, LCB-010-M1, LCB-010-M2, LCB-010-M3, LCB-010-M4, LCB-010-M5, LCB-011-M3, and LCB-011-M4 are all about 120 kD. The theoretical molecular weight of the control antibody Codrituzumab shown in Table 1 is 150 kD, the molecular weight of IFNα 2b-Fc is 88 kD, and the molecular weight of IFNα 2b monomer is 19.2 kD. The non-reducing SDS-PAGE protein electrophoresis assay results of the affinity captured (i.e., purified by Protein A) samples are shown in FIG. 3, and the reducing SDS-PAGE protein electrophoresis assay results are shown in FIG. 4. The electrophoresis results show that the antibody expressed by this structure contains many more aggregations. The non-reducing SDS-PAGE protein electrophoresis assay results after secondary purification (i.e., purified by SULFATE 650F) are shown in FIG. 5. It can be seen that most of the aggregations may be removed by cation exchange chromatography packing.

    [0198] After affinity capture, secondary purification of the other bispecific recombinant proteins shown in Table 1, the reducing and non-reducing SDS-PAGE protein electrophoresis assay results of the samples are consistent with the theoretical molecular weights, which will not be repeated herein.

    Embodiment 3: Assays of Affinity and Competitive Binding Activity to the Target of the Bispecific Recombinant Protein Whose Second Functional Antigen is CD47

    [0199] 1. Assay Method for Affinity of the Target CD47 and/or CD20

    [0200] Determination of Affinity of the Bispecific Recombinant Protein to the Target CD20 by Flow Cytometry:

    [0201] The binding affinity of the bispecific recombinant protein to the target CD20 was determined by flow cytometry. The following method takes LCB-001 or LCB-002 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is CD20.

    [0202] CHO-K1-hCD20 cells (hCD20-overexpressed Chinese hamster ovary epithelial cells) were cultured, well-grown cells were collected and counted, centrifuged and resuspended in PBS+2% FBS (purchased from Gibco) to a concentration of 3×10.sup.6 cells/mL. 100 μL of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and allowed to stand for at least 15 minutes; the plate was centrifuged and the supernatant was aspirated, then 8 dilution gradients of LCB-001, LCB-002, positive control Ofatumumab, positive control Rituximab, or negative control IgG (Isotype) (3-fold serial dilutions starting from 100 nM with 8 concentrations in total) were added respectively, and the 96-well plate was incubated in a refrigerator at 4° C. for 1 hour; after rinsing with PBS+2% FBS, goat anti-human IgG Fc-FITC (F9512-2ML, Sigma) was added and the plate was incubated at 4° C. for 1 hour; after rinsing and resuspension with PBS+2% FBS, the fluorescence value was determined by flow cytometry (BD).

    [0203] Since CHO-K1 cells do not express CD47 antigen, CHO-K1-hCD20 cells can be used to evaluate the binding affinity of the recombinant proteins LCB-001 and LCB-002, positive control samples Ofatumumab and Rituximab, and negative control IgG to CD20 at the cellular level.

    [0204] The results show that, except that the negative control IgG cannot bind to CHO-K1, the recombinant proteins LCB-001 and LCB-002, and the positive control samples Ofatumumab and Rituximab can all bind to CHO-K1 cells; the binding affinity of LCB-001 and LCB-002 to CD20 is similar to that of the anti-CD20 antibody Ofatumumab or Rituximab.

    [0205] The above experimental data prove that the recombinant protein of the present disclosure can specifically target the CD20 antigen of tumor cells at the cellular level, and the binding affinity to CD20 is not lower than the binding affinity of the monoclonal antibody with the same target to CD20; the recombinant protein of the present disclosure can target the target cells of interest with high affinity.

    [0206] For example, as shown in FIG. 6, the recombinant proteins LCB-001 and LCB-002, the positive control samples Ofatumumab and Rituximab can all bind to CHO-K1-hCD20 cells. Specifically, the binding affinity of LCB-001 and LCB-002 to CD20 is similar to that of the anti-CD20 antibody Ofatumumab or Rituximab.

    [0207] Determination of Affinity of the Bispecific Recombinant Protein to the Target CD47 by Flow Cytometry:

    [0208] The binding affinity of the bispecific recombinant protein to the target CD47 was determined by flow cytometry. The following method takes LCB-001, LCB-002, or LCB-017 as an example, and is suitable for the assay of the recombinant protein whose second functional antigen is CD47.

    [0209] HEK293 cells (human embryonic kidney cells 293) (CD20−/CD47+, non-target cells of interest) were cultured, well-grown cells were collected and counted, centrifuged and resuspended in PBS+2% FBS (Gibco) to a concentration of 3×10.sup.6 cells/mL. 100 μL of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and allowed to stand for at least 15 minutes; the plate was centrifuged and the supernatant was aspirated, then 7 dilution gradients of LCB-001, LCB-002, anti-CD47 antibody Magrolimab, anti-CD47 fusion protein TTI-621 or IgG1 (Isotype) (4-fold serial dilutions starting from 100 nM with 7 concentrations in total) were added respectively, and the 96-well plate was incubated in a refrigerator at 4° C. for 1 hour; after rinsing with PBS+2% FBS, goat anti-human IgG Fc-FITC (F9512-2ML, Sigma) was added and the plate was incubated at 4° C. for 1 hour; after rinsing and resuspension with PBS+2% FBS, the fluorescence value was determined by flow cytometry (BD).

    [0210] Since HEK293 cells do not express CD20 antigen, HEK293 cells can be used to evaluate the binding affinity of the bispecific recombinant proteins LCB-001 and LCB-002, positive control anti-CD47 antibody Magrolimab, anti-CD47 fusion protein TTI-621, and negative control IgG to CD47 at the cellular level.

    [0211] The results show that, except that the negative control IgG cannot bind to HEK293, the anti-CD47 antibody Magrolimab, anti-CD47 fusion protein TTI-621 (SIRPα D1-Fc fusion protein), recombinant proteins LCB-001 and LCB-002 can all bind to HEK293 cells; the binding of the recombinant proteins LCB-001 and LCB-002 to HEK293 is significantly weaker than that of the anti-CD47 antibody Magrolimab, and is also non-obviously weaker than that of the anti-CD47 fusion protein TTI-621.

    [0212] For example, as shown in FIG. 7A, the anti-CD47 antibody Magrolimab, the anti-CD47 fusion protein TTI-621, the recombinant proteins LCB-001 and LCB-002 were all able to bind to HEK293 cells. Specifically, the affinity of the recombinant proteins LCB-001 and LCB-002 was highly significantly weaker than that of the anti-CD47 antibody Magrolimab, and significantly weaker than that of the anti-CD47 fusion protein TTI-621 (SIRPα D1-Fc fusion protein).

    [0213] After CD47-transfected CHO-K1 cells (Chinese hamster ovary cells) (CD38−/CD47+, non-target cells of interest) were rinsed and digested, well-grown cells were collected and counted, centrifuged and resuspended in DPBS+2% FBS (Gibco) to a concentration of 3×10.sup.6 cells/mL. 100 μL of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning) and allowed to stand for at least 15 minutes; the plate was centrifuged and the supernatant was aspirated, then 7 dilution gradients of LCB-017, Felzartamab, TTI-621, or SIRPα-D1m-Fc (3-fold serial dilutions starting from 200 nM with 11 concentrations in total), and the 96-well plate was incubated in a refrigerator at 4° C. for 1 hour; after rinsing with DPBS+2% FBS, goat anti-human IgG Fc-FITC (F9512-2ML, Sigma) was added and the plate was incubated at 4° C. for 1 hour; after rinsing and resuspension with DPBS+2% FBS, the fluorescence value was determined by flow cytometry (BD).

    [0214] Since CD47-transfected CHO-K1 cells do not express CD38 antigen, the CHO-K1 cells can be used to evaluate the binding affinity of the bispecific recombinant protein LCB-017, the negative control anti-CD38 antibody Felzartamab, and the positive control anti-CD47 fusion protein TTI-621 and its high-affinity SIRPα D1m-Fc to CD47 at the cellular level.

    [0215] The results show that, except that the negative control anti-CD38 antibody Felzartamab cannot bind to CHO-K1, the anti-CD47 fusion protein TTI-621 (SIRPα D1-Fc fusion protein), high-affinity SIRPα D1m-Fc fusion protein and recombinant protein LCB-017 can all bind to HEK293 cells; the binding of the recombinant protein LCB-017 to non-target cell of interest CHO-K1 is significantly weaker than that of the anti-CD47 fusion protein TTI-621.

    [0216] For example, as shown in FIG. 7B, the high-affinity SIRPα D1m-Fc fusion protein, the anti-CD47 fusion protein TTI-621, and the recombinant protein LCB-017 can all bind to non-target cells of interest CHO-K1 cells. Specifically, the affinity of the recombinant protein LCB-017 is significantly weaker than that of the anti-CD47 fusion protein TTI-621 (SIRPα D1-Fc fusion protein).

    [0217] Other bispecific recombinant proteins of the present disclosure whose second functional antigen is CD47 can also be observed for their low binding affinity or no binding to non-target cells of interest.

    [0218] The above experimental data prove that the recombinant protein of the present disclosure can specifically target the CD47 antigen of tumor cells at the cellular level, and the binding affinity to CD47 is significantly weaker than that of the SIRPα D1-Fc fusion protein to CD47; the bispecific recombinant protein of the present disclosure can unexpectedly significantly reduce or avoid side effects including non-tumor target cell killings, such as hemagglutination, anemia, and thrombocytopenia which are produced by anti-CD47 antibody or SIRPα D1-Fc fusion protein treatment.

    [0219] Surface Plasmon Resonance Analysis (Hereafter “SPR Analysis”) on Affinity of the Bispecific Recombinant Protein to the Target CD20 or CD47:

    [0220] The following method takes LCB-002 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is CD20 and whose second functional antigen is CD47.

    [0221] Biacore T200 (GE Healthcare) was used for SPR Analysis. An anti-human IgG (Fc) antibody (Human Antibody Capture Kit, GE Healthcare) was immobilized on a CM5 sensor chip. 5 μg/mL of human CD20-Fc or human CD47-Fc chimeric proteins diluted with HBS-EP (GE Healthcare) were each allowed to immobilize, and the amount of capture was measured. Subsequently, the complete recombinant protein LCB-002, anti-CD20 antibody Ofatumumab, and anti-CD47 fusion protein TTI-621 were diluted to 50 nM with HBS-EP, and their binding capacities with human CD20-Fc chimeric protein or human CD47-Fc chimeric protein were measured respectively. Then, HBS-EP+buffer was added at a flow rate of 50 μL/min for 5 minutes, and the dissociation between the recombinant protein LCB-002, anti-CD20 antibody Ofatumumab, anti-CD47 fusion protein TTI-621 and human CD20-Fc chimeric protein or human CD47-Fc chimeric protein was measured. The bivalent analyte model and Rmax were analyzed by Fit local to calculate the association rate constant (ka) and the dissociation rate constant (kd), and the association-dissociation constant (KD) was calculated by dividing kd by ka. The Kd values of recombinant protein LCB-002, anti-CD20 antibody Ofatumumab, anti-CD47 fusion protein TTI-621 to human CD20-Fc chimeric protein or human CD47-Fc chimeric protein are shown in Table 3:

    TABLE-US-00003 TABLE 3 SPR Analysis on the association-dissociation constants of recombinant proteins or control samples to the first or second functional antigen Sample name Kd (hCD20) Kd (hCD47) LCB-002 3.24 nM 52.8 nM Ofatumumab 1.98 nM — TTI-621 — 37.3 nM

    [0222] Ofatumumab specifically targets the human CD20 protein, and therefore does not bind to the human CD47-Fc chimeric protein, while the anti-CD47 fusion protein TTI-621 specifically targets the CD47 protein, and therefore does not bind to the human CD20-Fc chimeric protein.

    [0223] The results show that at the protein level, the recombinant protein LCB-002 can bind to human CD47 protein or human CD20 protein, respectively, and its affinity does not change significantly compared with the anti-CD20 antibody Ofatumumab or the anti-CD47 fusion protein TTI-621.

    [0224] The above experimental data prove that the recombinant protein of the present disclosure can specifically target the CD20 antigen and CD47 antigen of tumor cells at the protein level, and the binding affinity to CD47 or CD20 is comparable to that of anti-CD20 antibody Ofatumumab or anti-CD47 fusion protein TTI-621.

    [0225] Determination of Bispecific Binding to the Targets CD20 and CD47 by Flow Cytometry:

    [0226] The binding affinity of the bispecific recombinant protein to the targets CD20 and CD47 was determined by flow cytometry. The following method takes LCB-001 or LCB-002 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is CD20 and whose second functional antigen is CD47.

    [0227] Well-grown Raji cells (human B-cell lymphoma) (Cell Bank of Chinese Academy of Sciences, Shanghai) (CD20+/CD47+, target cells of interest) were collected and counted, centrifuged and resuspended in PBS+2% FBS to a concentration of 3×10.sup.6 cells/mL. 100 pT, of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and 8 dilution gradients of LCB-001, LCB-002, Ofatumumab, Rituximab, IgG (3-fold serial dilutions starting from 100 nM with 8 concentrations in total) were added respectively, and the plate was incubated at 4° C. for 1 hour; after rinsing with PBS+2% FBS, goat anti-human IgG Fc-FITC (F9512-2ML, Sigma) was added and the plate was incubated at 4° C. for 1 hour; after rinsing and resuspension with PBS+2% FBS, the fluorescence value was determined by flow cytometry (BD).

    [0228] As shown in FIG. 8, since both CD20 and CD47 antigens are expressed on the surface of Raji cells, both anti-CD20 antibodies Ofatumumab and Rituximab can specifically bind to Raji cells, while the recombinant proteins LCB-001 and LCB-002 can also bind to Raji cells, and their binding abilities are similar to Ofatumumab and Rituximab.

    [0229] 2. Assay of Competitive Binding Activity to the Target

    [0230] The following method takes LCB-001, LCB-005, LCB-006, and LCB-017 as examples, and is suitable for the bispecific recombinant protein whose second functional antigen is CD47.

    [0231] Determination of Competitive Binding Activity of LCB-001 by Flow Cytometry:

    [0232] The competitive binding activity of the bispecific recombinant proteins LCB-001 and LCB-002 and the potential impurity control samples LCB-001-R and LCB-002-R, competing with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to CD47 on the cell surface was determined by flow cytometry. The following method takes LCB-001 or LCB-002 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is CD20 and whose second functional antigen is CD47.

    [0233] Well-grown Raji cells (human B-cell lymphoma) (Cell Bank of Chinese Academy of Sciences, Shanghai) were collected and counted, centrifuged and resuspended in PBS+2% FBS to a concentration of 3×10.sup.6 cells/mL. 100 μL of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and serially diluted LCB-001 (5-fold dilutions starting from a final concentration of 200,000 ng/mL with 8 concentration points in total) was added. The final concentration of FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) was 4 nM. LCB-001, SIRPα(CV1)-Fc-FITC and Raji cells were co-incubated for 1 hour, and the supernatant was discarded by centrifugation. The cells were resuspended with DPBS+2% FBS, and then determined by flow cytometry.

    [0234] The results show that anti-CD47 antibody Magrolimab, anti-CD47 fusion protein TTI-621, recombinant proteins LCB-001 and LCB-002 can compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc for binding to the CD47 antigen on Raji cells, and can exert competitive binding activity; potential impurities LCB-001-R and LCB-002-R cannot compete with FITC-labeled high-affinity SIRPα D1m-Fc for binding to the CD47 antigen, and cannot exert competitive binding activity.

    [0235] For example, as shown in FIG. 9A, anti-CD47 antibody Magrolimab, anti-CD47 fusion protein TTI-621, recombinant proteins LCB-001 and LCB-002 can compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc for binding to the CD47 antigen, and can exert competitive binding activity, and the competitive binding activity of the recombinant protein LCB-002 is non-obviously better than that of anti-CD47 fusion protein TTI-621, while the competitive binding activity of the recombinant protein LCB-001 is comparable to that of anti-CD47 fusion protein TTI-621. The results show that the recombinant protein using a suitable linker to connect the first functional structural fragment and the second functional structural fragment can non-obviously improve the competitive binding ability of the second functional structural fragment to the second functional antigen. At the same time, the potentially risky impurity proteins LCB-001-R and LCB-002-R cannot compete with FITC-labeled high-affinity SIRPα D1m-Fc for binding to the CD47 antigen. According to the results, the potentially risky impurities, which are generated during the preparation of recombinant proteins and are difficult to be completely removed, have significantly reduced the competitive binding activity to the second functional antigen. It can be inferred that the binding capability of the potentially risky impurities to the second functional antigen on non-target cells of interest is very weak, which greatly reduces the immune-related toxic side effects and has an excellent safety profile.

    [0236] Determination of Competitive Binding Activity of LCB-005 by Flow Cytometry:

    [0237] The competitive binding activity of the bispecific recombinant protein LCB-005, competing with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to CD47 on the cell surface was determined by flow cytometry. The following method takes LCB-005 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is EpCAM and whose second functional antigen is CD47.

    [0238] Well-grown target cells of interest CAPAN-2 cells (human pancreatic cancer cells) (EpCAM+/CD47+) (purchased from Nanjing Kebai) were rinsed and digested, counted, centrifuged and resuspended with DPBS+2% FBS to a concentration of 3×10.sup.6 cells/mL. 100 μL of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and the LCB-005 was serially diluted (3-fold dilutions starting from a final concentration of 200 nM with 8 concentration points in total). The final concentration of FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) was 4 nM. LCB-006, SIRPα D1m-Fc, TTI-621, SIRPα(CV1)-Fc-FITC, and CAPAN-2 cells were co-incubated for 1 hour, and the supernatant was discarded by centrifugation. The cells were resuspended with DPBS+2% FBS, and then determined by flow cytometry.

    [0239] The results show that, compared with the anti-CD47 fusion protein TTI-621, which has no obvious competitive binding activity on CAPAN-2 cells, both the bispecific recombinant protein LCB-005 and the high-affinity SIRPα D1m-Fc can compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to the CD47 antigen on CAPAN-2 cells, and can exert competitive binding activity. The competitive binding capability of the bispecific recombinant protein LCB-005 to CAPAN-2 is significantly better than that of the anti-CD47 fusion protein TTI-621.

    [0240] For example, as shown in FIG. 9B, both the bispecific recombinant protein LCB-005 and the high-affinity SIRPα D1m-Fc can compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to the CD47 antigen, and can exert competitive binding activity, while the competitive binding activity of anti-CD47 fusion protein TTI-621 is not observed. It can be seen that the competitive binding activity of the bispecific recombinant protein LCB-005 is non-obviously better than that of anti-CD47 fusion protein TTI-621. The results show that the bispecific recombinant protein of the present disclosure using a suitable linker to connect the first functional structural fragment and the second functional structural fragment can non-obviously improve the competitive binding ability of the second functional structural fragment to the second functional antigen.

    [0241] Determination of Competitive Binding Activity of LCB-006 by Flow Cytometry:

    [0242] The competitive binding activity of the bispecific recombinant protein LCB-006, competing with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to CD47 on the cell surface was determined by flow cytometry. The following method takes LCB-006 as an example, which is suitable for the assay of the recombinant protein whose first functional antigen is CD24 and whose second functional antigen is CD47.

    [0243] Well-grown target cells of interest MCF-7 cells (human breast cancer cells) (CD24+/CD47+) (purchased from Nanjing Kebai) were rinsed and digested, counted, centrifuged and resuspended with DPBS+2% FBS to a concentration of 3×10.sup.6 cells/mL. 100 μL of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and the LCB-006 was serially diluted (3-fold dilutions starting from a final concentration of 200 nM with 8 concentration points in total). The final concentration of FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) was 4 nM. LCB-006, SIRPα D1m-Fc, TTI-621, SIRPα(CV1)-Fc-FITC and MCF-7 cells were co-incubated for 1 hour, and the supernatant was discarded by centrifugation. The cells were resuspended with DPBS+2% FBS, and then determined by flow cytometry.

    [0244] The results show that, compared with the anti-CD47 fusion protein TTI-621, which has no obvious competitive binding activity on MCF-7 cells, both the bispecific recombinant protein LCB-006 and the high-affinity SIRPα D1m-Fc can compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to the CD47 antigen on MCF-7 cells, and can exert competitive binding activity. The competitive binding activity of the bispecific recombinant protein LCB-006 to MCF-7 is significantly better than that of the anti-CD47 fusion protein TTI-621.

    [0245] For example, as shown in FIG. 9C, both the bispecific recombinant protein LCB-006 and the high-affinity SIRPα D1m-Fc can compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to the CD47 antigen, and can exert competitive binding activity, while the competitive binding activity of anti-CD47 fusion protein TTI-621 is not observed. It can be seen that the competitive binding activity of the bispecific recombinant protein LCB-006 is non-obviously better than that of anti-CD47 fusion protein TTI-621. The results show that the bispecific recombinant protein of the present disclosure using a suitable linker to connect the first functional structural fragment and the second functional structural fragment can non-obviously improve the competitive binding ability of the second functional structural fragment to the second functional antigen.

    [0246] Determination of Competitive Binding Activity of LCB-017 by Flow Cytometry:

    [0247] The competitive binding activity of the bispecific recombinant protein LCB-017, competing with FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) for binding to CD47 on the cell surface was determined by flow cytometry. The following method takes LCB-017 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is CD38 and whose second functional antigen is CD47.

    [0248] Well-grown Raji cells (human B-cell lymphoma) (Cell Bank of Chinese Academy of Sciences, Shanghai) (CD38+/CD47+) were collected, counted and centrifuged, and the cells were resuspended with DPBS+2% FBS to a concentration of 3×10.sup.6 cells/mL. 100 μL of a cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and the LCB-017 was serially diluted (3-fold dilutions starting from a final concentration of 200 nM with 7 concentration points in total). The final concentration of FITC-labeled high-affinity SIRPα D1m-Fc (SIRPα(CV1)-Fc-FITC) was 4 nM. LCB-017, SIRPα D1m-Fc, TTI-621, SIRPα(CV1)-Fc-FITC and Raji cells were co-incubated for 1 hour, and the supernatant was discarded by centrifugation. The cells were resuspended with DPBS+2% FBS, and then determined by flow cytometry.

    [0249] The results show that anti-CD47 fusion protein TTI-621, the bispecific recombinant protein LCB-017 and high-affinity SIRPα D1m-Fc can all compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc for binding to the CD47 antigen on Raji cells, and exert competitive binding activity. The competitive binding activity of the bispecific recombinant protein LCB-017 to MCF-7 is significantly better than that of the anti-CD47 fusion protein TTI-621.

    [0250] For example, as shown in FIG. 9D, anti-CD47 fusion protein TTI-621, the bispecific recombinant protein LCB-017, and high-affinity SIRPα D1m-Fc can all compete in varying degrees with FITC-labeled high-affinity SIRPα D1m-Fc for binding to the CD47 antigen on Raji cells, and exert competitive binding activity. It can be seen that the competitive binding activity of the bispecific recombinant protein LCB-017 (IC50=27.98) is non-obviously better than that of the anti-CD47 fusion protein TTI-621 (IC50=1067). The results show that the bispecific recombinant protein of the present disclosure using a suitable linker to connect the first functional structural fragment and the second functional structural fragment can non-obviously improve the competitive binding ability of the second functional structural fragment to the second functional antigen.

    [0251] To sum up (FIG. 9A-FIG. 9D), the bispecific recombinant protein of the present disclosure using a suitable linker to connect the first functional structural fragment and the second functional structural fragment can non-obviously improve the competitive binding ability of the second functional structural fragment to the second functional antigen. The results are also observed in other bispecific recombinant proteins whose second functional antigen is CD47 on target cells of interest with positive antigen of interest, which are consistent with the above data.

    Embodiment 4: Binding Activity Assay of GPC3-Targeted Bispecific Recombinant Proteins to Liver Cancer Cell Lines Highly Expressed with GPC3 (Double-Positive Expressing Cells, Target Cells of Interest)

    [0252] The binding affinity of the GPC3-targeted bispecific recombinant protein to the liver cancer cell line highly expressed with the target GPC3 was determined by flow cytometry. The following method takes LCB-009, LCB-010, and LCB-011 as examples, and is suitable for the assay of the bispecific recombinant protein whose first functional binding fragment binds to GPC3 antigen and whose second functional binding fragment is IFN-α 2b or its low-affinity mutant.

    [0253] The cells for the assay were HepG2 cells (Nanjing Kebai Biotechnology Co., Ltd.) and HuH-7 (Cell Bank of Chinese Academy of Sciences, Shanghai). Well-grown cells were collected and counted, centrifuged and resuspended in FACS buffer (PBS+2% FBS) to a concentration of 1×10.sup.6 cell s/mL. 100 μL of the cell suspension was aliquoted to each well of a 96-well U-shaped plate (Art. No. 3799, Corning), and 7 dilution gradients of bispecific recombinant proteins or control proteins (3-fold serial dilutions starting from 100 nM with 7 concentrations in total) were added respectively, and the plate was incubated at 4° C. for 1 hour; after rinsing with FACS buffer, goat anti-human IgG (Alexa Fluor488 goat anti-human IgG (H+L), Invitrogen) was added and the plate was incubated at 4° C. for 1 hour; after rinsing and resuspension with FACS buffer, the fluorescence value was determined by flow cytometer (Attune Nxt, Invitrogen).

    [0254] The results are shown in FIG. 10 and FIG. 11. The bispecific recombinant proteins LCB-009, LCB-010, and LCB-011 all have a certain degree of binding activity with the target cells of interest HepG2 and HuH-7 cells that express GPC3 and IFNα receptors simultaneously, and the binding of the bispecific recombinant protein to HepG2 and HuH-7 cells has a higher maximum average fluorescence intensity than that of anti-GPC3 mAb (control sample Codrituzumab). At the same time, as shown in FIG. 10 and FIG. 11, the length of the linker has a weak effect on the binding activity of the bispecific recombinant protein to the target cells of interest. When the linker is short (for example, the linker sequence is one GGGGS), the binding activity (EC50) of bispecific recombinant proteins (such as LCB-009) to target cells of interest is relatively low.

    Embodiment 5: Activity Assay of Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) of GPC3-Targeted Bispecific Recombinant Protein

    [0255] The ADCC activity of the bispecific recombinant protein on the hepatoma cell line highly expressed with the target GPC3 was determined by lactate dehydrogenase (LDH) method. The following method takes LCB-009, LCB-010, and LCB-011 as examples, and is suitable for the bispecific recombinant protein whose first functional binding fragment binds to GPC3 antigen and whose second functional binding fragment is IFN-α 2b or its low-affinity mutant.

    [0256] Human peripheral blood mononuclear cells (PBMC) were used as effector cells, the target cells of interest were HepG2 liver cancer cell line highly expressed with GPC3, and the LDH assay kit was CytoTox-ONETM-Homogeneous Membrance Integrity Assay, Promega, G7892. Target cells of interest and effector cells were plated at a ratio of 1:20, then bispecific recombinant proteins or control proteins (5-fold serial dilutions starting from 150 nM with 8 concentrations in total) were added, and the plate was incubated at 37° C. for 4 hours. After incubation at 37° C. for 3.5 hours, lysis reagent was added to the control group, and the cells were observed under a microscope. After the cells were completely lysed, they were centrifuged at 10,000 rpm for 5 minutes. The supernatant was transferred to a 96-well black-bottomed transparent plate (Corning, 3904), and incubated with the reaction substrate at 37° C. for 30 minutes. The termination solution was then added, and the plate was shaked in the dark for 3 to 5 minutes. The signal value was detected by the microplate reader (SpectraMax M2), and the detailed steps were referred from the LDH assay kit instructions.

    [0257] As shown in FIG. 12, the bispecific recombinant protein (such as LCB-009, LCB-010, LCB-011) retains ADCC activity, and the ADCC activity of the bispecific recombinant protein is comparable to that of anti-GPC3 mAb (control sample Codrituzumab) (EC50=0.53).

    Embodiment 6: Assay of Proliferation Inhibition Activity of GPC3-Targeted Bispecific Recombinant Protein

    [0258] The proliferation inhibition activities of the GPC3-targeted bispecific recombinant protein on different tumor cell lines were determined by cell titer glo kit (Promega, Cat: G7558). The following method takes LCB-009, LCB-010, and LCB-011 as examples, and is suitable for the assay of the bispecific recombinant protein whose first functional binding fragment binds to GPC3 antigen and whose second functional binding fragment is IFNα 2b or its low-affinity mutant.

    [0259] GPC3-positive cell line HuH-7 or GPC3-negative tumor cell line U266 (purchased from Nanjing Kebai Biotechnology Co., Ltd.) and GPC3-negative tumor cell line SW480 (purchased from Nanjing Kebai Biotechnology Co., Ltd.) were plated in a 96-well black-bottomed transparent plate (Corning, 3904), then bispecific recombinant proteins or control proteins (10-fold serial dilutions starting from 52 nM with 6 points in total; or 5-fold serial dilutions starting from 10 nM with 8 points in total) were added, and the plate was incubated in a carbon dioxide incubator at 37° C. for 3 days. Cell titer glo was added, and the signal value was detected by Multomode Plate Reader (PerkinElmer, Envision2105).

    [0260] The results show that the proliferation inhibition activity (IC50) of the bispecific recombinant protein (such as LCB-009, LCB-010, LCB-011) on GPC3-positive (GPC3+) target cells of interest HuH-7 is higher than that of the control IFN-α 2b (as shown in FIG. 13), and is higher than that of the anti-GPC3 mAb (i.e. the control sample Codrituzumab, the proliferation inhibition effect of this antibody on HuH-7 is not observed) as well. As shown in FIG. 14, the proliferation inhibition activities of the bispecific recombinant protein LCB-012 lacking the function of targeting GPC3 and the Fc fusion protein of IFN-α2b (IFN-α2b-Fc) on HuH-7 (GPC3-positive target cells of interest) are significantly lower than that of the bispecific recombinant protein LCB-010 with the function of targeting GPC3, indicating that the binding of the bispecific recombinant protein with the function of targeting GPC3 to GPC3 on target cells of interest can significantly enhance the proliferation inhibition activity of IFN-α 2b, but IFN-α2b of the bispecific recombinant protein without the effect of targeting the target cells of interest has a low proliferation inhibition activity. It reveals that the bispecific recombinant protein of the present disclosure has a strong proliferation inhibition effect only on the target cells of interest with the antigen of interest, but has a weak effect on or does not bind to the non-target cells of interest without the antigen of interest, indicating that the bispecific recombinant protein of the present disclosure has a high safety profile.

    [0261] In addition, as shown in Table 4, compared with IFN-α 2b, the bispecific recombinant proteins with different linkers (taking LCB-009, LCB-010, LCB-011 as examples) have stronger proliferation inhibition activities on GPC3-positive (GPC3+) target cells of interest (taking HuH-7 as an example), and the proliferation inhibition activities of the bispecific recombinant proteins with different linkers differ slightly. The bispecific recombinant protein containing one GGGGS as the linker sequence (i.e. the bispecific recombinant protein connected by a shorter linker) (taking LCB-009 as an example) has relatively low activity (as shown in FIG. 13 and Table 4), which is consistent with the results of binding activities of the recombinant proteins with different linkers as shown in FIG. 11. But in GPC3-negative (GPC3−) non-target cells of interest U266 and SW480 cell lines, the proliferation inhibition activities of the bispecific recombinant proteins (taking LCB-009, LCB-010, LCB-011 as examples) are significantly lower than that of IFN-α2b (that is, the relative activity of the bispecific recombinant protein is much less than 1), which indicates that in cells that do not express GPC3 (i.e. non-target cells of interest that do not express the antigen of interest), the proliferation inhibition activity of the bispecific recombinant protein is very low, suggesting a high safety profile. At the same time, as shown in Table 4, the proliferation inhibition activity of the bispecific recombinant protein on target cells of interest is at least 700 times higher than that of the bispecific recombinant protein on non-target cells of interest.

    TABLE-US-00004 TABLE 4 The relative proliferation inhibition activities of bispecific recombinant proteins with different linkers Relative activity Relative activity ratio (IC50 IFN-α 2b/bispecific (target cell of interest/ recombinant protein) non-target cell of interest) HuH-7 U266 SW480 HuH-7(GPC3+)/ HuH-7(GPC3+)/ Sample (GPC3+) (GPC3−) (GPC3−) U266(GPC3−) SW480(GPC3−) LCB-009 17.80 0.008 0.023 2225.000 773.913 LCB-010 27.00 0.034 0.017 794.118 1588.235 LCB-011 23.40 0.004 0.030 5850.000 780.000

    Embodiment 7: Assay of Proliferation Inhibition Activity of PD-L1-Targeted Bispecific Recombinant Protein

    [0262] The proliferation inhibition activities of the PD-L1-targeted bispecific recombinant protein on different tumor cell lines were determined by cell titer glo kit (Promega, Cat: G7558). The following method takes LCB-013, LCB-014, and LCB-015 as examples, and is suitable for the bispecific recombinant protein whose first functional binding fragment binds to PD-L1 antigen and whose second functional binding fragment is IFN-α 2b or its low-affinity mutant.

    [0263] PD-L1 positive cell line MDA-MB-231 (purchased from Nanjing Kebai Biotechnology Co., Ltd.) was plated in a 96-well black-bottomed transparent plate (Corning, 3904), then bispecific recombinant proteins or control proteins (10-fold serial dilutions starting from 52 nM with 6 concentration points in total) were added, and the plate was incubated in a carbon dioxide incubator at 37° C. for 3 days. Cell titer glo was added, and the signal value was detected by Multomode Plate Reader (PerkinElmer, Envision2105).

    [0264] As shown in FIG. 15, for PD-L1-positive (PD-L1+) target cells of interest MDA-MB-231, PD-L1-targeted bispecific recombinant proteins (LCB-013, LCB-014, LCB-015) all have proliferation inhibition activity, and the activity is significantly higher than the control bispecific recombinant protein LCB-012 without the function of targeting PD-L1 and IFN-α 2b, indicating that targeting PD-L1 can significantly enhance the proliferation inhibition activity of IFN-α2b. It is shown that the bispecific recombinant protein with the function of targeting PD-L1 binding to PD-L1 on the target cell of interest MDA-MB-231 can significantly enhance the proliferation inhibition activity of IFN-α2b, but the proliferation inhibition activity of IFN-α2b of the bispecific recombinant protein without the function of targeting the target cell of interest is relatively low. It reveals that the bispecific recombinant protein of the present disclosure has a strong proliferation inhibition effect only on the target cells of interest with the antigen of interest, but has a weak effect on or does not bind to the non-target cells of interest that do not express the antigen of interest, indicating that the bispecific recombinant protein of the present disclosure has a high safety profile.

    [0265] PD-L1-positive target cells of interest MDA-MB-231 were plated in a 96-well black-bottomed transparent plate (Corning, 3904), then 200 nM of PD-L1 antibody Atezolizumab or isotype control was added, and the plate was incubated at 37° C. for 30 minutes. Bispecific recombinant proteins or control proteins (6-fold dilutions starting from a concentration of 20 nM with 6 concentration points in total) were added, and the plate was incubated in a carbon dioxide incubator at 37° C. for 3 days. Cell titer glo was added, and the signal value was detected by Multomode Plate Reader (PerkinElmer, Envision2105).

    [0266] As shown in FIG. 16, after Atezolizumab was added to block the binding site of PD-L1 antigen and the antibody, the proliferation inhibition activity of LCB-015 was significantly reduced. The results prove that blocking the binding function of the antigen of interest on the cells to be tested results in a significant decrease in the proliferation inhibition activity of the bispecific recombinant protein on the cells to be tested, which demonstrates from another perspective that the bispecific recombinant protein of the present disclosure has a weak effect on or does not bind to non-target cells of interest without the ability to bind to the antigen of interest, indicating that the bispecific recombinant protein of the present disclosure has a high safety profile.

    Embodiment 8: Assay of Proliferation Inhibition Activity of CD38-Targeted Bispecific Recombinant Protein

    [0267] The proliferation inhibition activities of the CD38-targeted bispecific recombinant protein on different tumor cell lines were determined by cell titer glo kit (Promega, Cat: G7558). The following method takes LCB-016 as an example, and is suitable for the assay of the bispecific recombinant protein whose first functional binding fragment binds to CD38 antigen and whose second functional binding fragment is IFNα2b.

    [0268] CD38-positive cell line Daudi or CD38-negative tumor cell line SK-BR-3 (purchased from Nanjing Kebai Biotechnology Co., Ltd.) was plated in a 96-well black-bottomed transparent plate (Corning, 3904), then bispecific recombinant proteins or control proteins (5-fold serial dilutions starting from 2 nM with 9 points in total) were added, and the plate was incubated in a carbon dioxide incubator at 37° C. for 3 days. Cell titer glo was added, and the signal value was detected by Multomode Plate Reader (PerkinElmer, Envision2105).

    [0269] The results show that the proliferation inhibition activity (IC50) of the bispecific recombinant protein (such as LCB-016) on the CD38-positive (CD38+) target cell of interest Daudi is non-obviously stronger than that of the control IFN-α 2b (as shown in FIG. 17A), relatively speaking, the proliferation inhibition activity (IC50) of the bispecific recombinant protein (such as LCB-016) on the CD38-negative (CD38−) non-target cell of interest SK-BR3 is non-obviously weaker than that of the control IFN-α 2b (as shown in FIG. 17B). That is, while the proliferation inhibition activity of IFNα 2b in the bispecific recombinant protein whose second functional binding fragment is IFNα 2b on the target cells of interest with the antigen of interest is enhanced, the proliferation inhibition effect of IFNα 2b in the bispecific recombinant protein on the non-target cells of interest without the antigen of interest is significantly reduced. It is revealed that the bispecific recombinant protein of the present disclosure has a strong proliferation inhibition effect only on the target cells of interest with the antigen of interest, but has a weak effect on or does not bind to the non-target cells of interest without the antigen of interest, indicating that the bispecific recombinant protein of the present disclosure has a high safety profile.

    [0270] As shown in FIG. 17A, the CD38-targeted bispecific recombinant protein (LCB-016) has proliferation inhibition activity on the CD38-positive (CD38+) target cell of interest Daudi, and the activity is significantly higher than that of IFN-α 2b without the function of targeting CD38, indicating that targeting CD38 can significantly enhance the proliferation inhibition activity of IFN-α 2b. It is shown that the bispecific recombinant protein with the function of targeting CD38 binding to CD38 on the target cell of interest Daudi can significantly enhance the proliferation inhibition activity of IFN-α 2b. As shown in FIG. 17B, the proliferation inhibition activity of IFN-α 2b lacking the function of targeting CD38 on SK-BR3 (CD38-negative non-target cell of interest) is significantly stronger than that of the bispecific recombinant protein LCB-016 with the function of targeting CD38, indicating that IFN-α 2b of the bispecific recombinant protein exerts a low proliferation inhibition activity on non-target cells of interest without the antigen of interest. The relative activity of LCB-016 to IFN-α 2b on the target cell of interest Daudi is at least 200 times higher than that on the non-target cell of interest SK-BR3.

    Embodiment 9: Assay of Proliferation Inhibition Activity of the Bispecific Recombinant Protein Containing IFN-α 2b Low-Affinity Mutant

    [0271] Considering the difference between the human body-tolerated dose of IFN-α 2b and the effective dose of conventional antibodies, in order to better match the effect of the antigen of interest-targeted antigen-binding fragment and IFN-α 2b, and achieve the effect of high efficiency and low toxicity, the present disclosure also designed a series of bispecific recombinant proteins containing IFN-α 2b low-affinity mutants. This embodiment takes the mutation design based on LCB-010 as an example to design the bispecific recombinant proteins containing IFN-α 2b low-affinity mutants, and to determine the proliferation inhibition activity of the bispecific recombinant proteins containing different IFN-α 2b low-affinity mutants. The experimental method is the same as Embodiment 7.

    [0272] As shown in FIG. 18-FIG. 20, the results show that the proliferation inhibition activities of the bispecific recombinant proteins with IFN-α 2b low-affinity mutants LCB-010-M2, LCB-010-M3 and LCB-010-M4 on GPC3-positive target cells of interest (HuH-7) or GPC3-negative non-target cells of interest (U266, SW480) are all lower than that of LCB-010. For example, the proliferation inhibition activity IC50 of LCB-010-M3 (A145G mutation) on HuH-7 (GPC3-positive cell line, target cell of interest) is comparable to that of IFN-α 2b (IC50.sub.IFN-α 2b=0.1793, IC50.sub.LCB-010-M3=0.179), but the relative proliferation inhibition activity (IC50 IFN-α 2b/bispecific recombinant protein) of LCB-010-M3 on GPC3-negative non-target cell of interest (U266) is weaker, e.g., the relative proliferation inhibition activity (IC50 IFN-α 2b/bispecific recombinant protein) of LCB-010-M3 on U266 is 0.000615, which is significantly lower than that of IFN-α 2b and lower than that of LCB-010, and LCB-010-M4 (R149A mutation) also has similar results.

    [0273] The above results and FIG. 19-FIG. 21 show that the activity of the GPC3-targeted bispecific recombinant protein containing the IFN-α 2b low-affinity mutant in the target cell line with positive antigen of interest is comparable to that of IFN-α 2b, but the activity decreases in the non-target cell line that does not express the antigen of interest, suggesting a higher safety profile of the bispecific recombinant protein containing the IFN-α 2b low-affinity mutant of the present disclosure.

    [0274] In summary, the degree of decrease in the proliferation inhibition activity of the bispecific recombinant protein containing the IFN-α 2b low-affinity mutant of the present disclosure relative to the bispecific recombinant protein containing wild-type IFN-α 2b on non-target cells of interest with negative antigen of interest, is comparable to or more significant than the degree of decrease in the proliferation inhibition activity of the bispecific recombinant protein containing the IFN-α 2b low-affinity mutant on non-target cells of interest with negative antigen of interest relative to that on target cells of interest with positive antigen of interest.

    Embodiment 10: Assay of Proliferation Inhibition Activity of Potentially Risky Impurities of the Bispecific Recombinant Protein on Non-Target Cell of Interest

    [0275] In order to reduce the potential safety risk of impurities in the future preparation process of the bispecific recombinant protein, the present disclosure takes LCB-010 as an example to analyze the proliferation inhibition of potentially risky impurities (chain B homodimer) on non-target cells of interest.

    [0276] In the secondary purification process of LCB-010 (as described in Embodiment 2), the chain B homodimer of LCB-010 (FIG. 3, the molecular weight of the homodimer is about 140 kD) was isolated, and the proliferation inhibition activities of the potentially risky impurity and IFN-α 2b-Fc (the potentially risky impurity of the bi-clonal antibody structure shown in FIG. 3A of CN108864290A, the right arm homodimer with D1 replaced by IFN-α 2b) on non-target cells of interest (GPC3-negative cells) MDA-MB-231 were determined. The results are shown in FIG. 21 that, at the concentration of 16.7 nM, the proliferation inhibition rate of IFN-α 2b on MDA-MB-231 (GPC3-negative cell, non-target cell of interest) is 91.3%, the inhibition rate of IFN-α 2b-Fc on MDA-MB-231 (GPC3-negative cell, non-target cell of interest) is 66.8% (reduced by about 24.5% compared with IFN-α 2b), while the proliferation inhibition rate of the chain B homodimer of LCB-010 on MDA-MB-231 (GPC3-negative cell, non-target cell of interest) is only 16.2% (reduced by about 75.1% compared with IFN-α 2b, and reduced by about 50% compared with IFN-α 2b-Fc). To sum up, the potentially risky impurities only have a very weak effect on non-target cells of interest, that is, the potential safety risks or potential toxic side effects are very low.

    Embodiment 11: Assay of Target Affinity of the Bispecific Recombinant Protein Whose Second Functional Binding Fragment is IL12

    [0277] The binding affinity of the bispecific recombinant protein to the target TIGIT and IL12 receptors was determined by flow cytometry. The following method takes LCB-018 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is TIGIT and whose second functional binding fragment is IL12A.

    [0278] H_IL12 Reporter 293 cells (TIGIT+, target cells of interest) were plated in a 96-well white-walled and -bottomed transparent plate (Corning, 3903), and after the cells were adhered overnight, the medium was discarded. 200 nM of anti-TIGIT monoclonal antibody Tiragolumab or isotype control antibody was added, the plate was incubated at 37° C. for 30 minutes, and the medium was discarded. 200 nM of the bispecific recombinant protein LCB-018 and 2 μg/mL of IL12B were mixed thoroughly in equal volume, the mixture was 3-fold diluted downward with 10 concentration points in total, then added to a 96-well plate as 150 μL/well, and the plate was incubated in a carbon dioxide incubator at 37° C. for 6 hours. One-Glo was added, and the signal value was detected by Multomode Plate Reader (PerkinElmer, Envision 2105).

    [0279] The results show that (as shown in FIG. 22), with anti-TIGIT monoclonal antibody Tiragolumab added to block TIGIT, the binding curve of the bispecific recombinant protein and the cells to be tested was obviously shifted to the right, which proved that the bispecific recombinant protein of the present disclosure using a suitable linker to connect the first functional structural fragment (the part targeting TIGIT) and the second functional structural fragment (IL12) may non-obviously improve the binding ability of the bispecific recombinant protein to the target cells. In addition, for the target cell with positive antigen, the binding affinity of the bispecific recombinant protein of the present disclosure (such as LCB-018) to this target cell (such as H_IL12 Reporter 293 cell) was about 500 times weaker than that of the IL12A and IL12B complex at the same concentration to the same cell (EC50.sub.LCB-018=30 nM, EC50.sub.IL12A/IL12B=0.06 nM), which also proved that the targeting effect of the bispecific recombinant protein of the present disclosure may significantly reduce the binding activity of IL12 to cells, thus reducing the potential toxic side effects of IL12, especially the toxic side effects of IL12 binding to non-target cells.

    Embodiment 12: Assay of P-STAT3 Activation Level in THP1 Cells by the Bispecific Recombinant Protein Whose Second Functional Binding Fragment is IL10M

    [0280] The assay of P-STAT3 activation levels in THP1 cells by the bispecific recombinant protein was determined by flow cytometry. The following method takes LCB-019 as an example, and is suitable for the assay of the recombinant protein whose first functional antigen is CD80 and whose second functional binding fragment is IL10M.

    [0281] LCB-019, LCB-022 (control bispecific recombinant protein can not bind to CD80), Isotype, and IL10M-Fc fusion protein were diluted with a basal medium (1640) at an equimolar concentration of 106 nM for use.

    [0282] Considering that LPS (sigma, L5418-2ML) can stimulate the expression of CD80 antigen on the surface of Thp1 cells (sourced from Cell Bank of Chinese Academy of Sciences), this embodiment utilized Thp1 cells stimulated by LPS for 24 hours to simulate the target CD80-positive cells (target cells of interest).

    [0283] Thp1 cells (sourced from Cell Bank of Chinese Academy of Sciences) stimulated by 1 μg/mL of LPS (sigma, L5418-2ML) for 24 hours were resuspended in a basal medium (1640) at a density of 1×10.sup.6. The resuspended cells stimulated by LPS and Thp1 cells not stimulated by LPS were plated in a 96-well plate as a volume of 100 μL, and equal volumes of diluted LCB-019, LCB-022 (control bispecific recombinant protein), Isotype, IL10M-Fc fusion protein were added and the plate was incubated in a 37° C., 5% carbon dioxide incubator for 20 minutes. After incubation, the supernatant was removed by centrifugation, and the cells were immobilized and treated with membrane permeabilization. The cells were then resuspended in 100 μL of FACS buffer (1×PBS+2% FBS) containing 0.5 μL of PE-P-STAT3 antibody (BD, 562072) and incubated in the dark at 4° C. for 1 hour. After washed twice with FACS buffer (1×PBS+2% FBS), the cells were resuspended with the addition of 200 μL of FACS buffer (1×PBS+2% FBS), and the P-STAT3 level was detected by FACS.

    [0284] The results as shown in FIG. 23, on Thp1 cells highly expressing the antigen CD80 after LPS stimulation, the P-STAT3 level of LCB-019, a bispecific recombinant protein was basically comparable to that of IL10M-Fc fusion protein and significantly higher than that of LCB-022, a control bispecific recombinant protein without targeting function, while on Thp1 cells not stimulated by LPS, the P-STAT3 levels of LCB-019 and control bispecific recombinant protein LCB-022 were basically comparable and significantly weaker than that of IL10M-Fc fusion protein.

    [0285] It can be seen that, for non-target cells with weak or no expression of the antigen, the effect of the bispecific recombinant protein on non-target cells is significantly weaker than that of IL10M-Fc fusion protein, showing its relatively higher safety profile. Whereas for the target cells with high antigen expression, the bispecific recombinant protein targeting the antigen may show a STAT3 level that is comparable to that of the IL10M-Fc fusion protein, and may fully exert and improve the efficacy of IL10M in the bispecific recombinant protein. On the contrary, the bispecific recombinant protein without the function of targeting the antigen has a relatively weak effect on the cells (non-target cells), showing a good safety profile.

    Embodiment 13: Assay of the Proliferation Activity of the Bispecific Recombinant Protein Whose Second Functional Binding Fragment is IL15-IL15RαSUSHI

    [0286] The proliferation capability of bispecific recombinant protein on PD-1-positive hPBMCs stimulated by OKT3 for 48 hours was determined by flow cytometry. The following method takes LCB-020, LCB-021, LCB-023, and LCB-024 as examples, and is suitable for the assay of the recombinant protein whose first functional antigen is PD-1 and whose second functional binding fragment is IL15-IL15RαSUSHI.

    [0287] The hPBMC cells were recovered and put into a 6-well plate pre-coated with 100 ng/mL of anti-CD3 antibody (OKT3, eBioscience, Cat. #16-0037-85), and incubated for 48 hours. Activated PBMCs were collected by centrifugation and washed once with PBS. The cells were then resuspended in a culture medium, plated into a 96-well plate at a density of 1.5E5/100 μL/well, and 1.6 nM of positive control C15Y, bispecific recombinant proteins LCB-020, LCB-021, LCB-023 and LCB-024 were added. The 96-well plate was incubated in a carbon dioxide incubator at 37° C. for 96 hours. After incubation, for cell sorting, the cell membranes were first stained with anti-CD4-APC (eBioscience, Cat. #17-0049-42) and anti-CD8-FITC (Invitrogen, Cat. #MHCD0801) antibodies. After staining, the cells were permeabilized with a fixed permeabilization reagent (eBioscience™ Foxp3/Transcription Factor Staining Buffer Set. Invitrogen, Cat. #00-5523-00). After permeabilization, the cells were stained with anti-Ki-67-PE (Biolegend, Cat. #350504) antibody for 40 minutes. The expression of Ki-67 on CD4+ and CD8+ cell populations was analyzed by FACS at the end of staining.

    [0288] As shown in FIG. 24, all of the 5 samples have a certain pro-proliferation effect on hPBMCs with high PD-1 expression at a concentration of 1.6 nM. Among them, the positive control C15Y has the strongest activity, the pro-proliferation effects of the bispecific recombinant proteins LCB-020 and LCB-021 with the function of targeting PD-1, and the control bispecific recombinant proteins RSV×IL-15R antibodies (LCB-023, LCB-024) without the function of targeting PD-1, are weaker than that of the positive control C15Y. And the pro-proliferation effect of the bispecific recombinant proteins LCB-020 and LCB-021 with the function of targeting PD-1 is obviously stronger than that of the control bispecific recombinant proteins LCB-023 and LCB-024 without the function of targeting PD-1. At the same time, the pro-proliferation effect of the control bispecific recombinant proteins LCB-023 and LCB-024 without the function of targeting PD-1 is weak. The results show that the bispecific recombinant protein with the function of targeting the antigen may significantly enhance the pro-proliferation effect of IL15-IL15RαSUSHI on the target cells, and the pro-proliferation effect is weaker than that of the IL15-IL15RαSUSHI-Fc fusion protein (C15Y); the control bispecific recombinant protein pair (LCB-023, LCB-024) has a weak pro-proliferation effect on PD-1-positive hPBMCs stimulated by OKT3 for 24 hours, which reveals from another perspective that the bispecific recombinant protein of the present disclosure has a weak effect on non-target cells that do not express the antigen, demonstrating its high safety profile.

    [0289] The proliferation activity of the PD-1-targeted bispecific recombinant protein on M-07e was determined by cell titer glo kit (Promega, Cat: G7558). The following method takes LCB-020, LCB-021, LCB-023, and LCB-024 as examples, and is suitable for the assay of the recombinant protein whose first functional antigen is PD-1 and whose second functional binding fragment is IL15-IL15RαSUSHI.

    [0290] Cytokine-dependent cells M-07e were collected and washed once with PBS. The cells were diluted to a density of 2E4/50 μL with a medium not containing GM-CSF (R&D, Cat. #215-GM-050) growth factor, plated into a 96-well plate, and incubated for 4 hours for cytokine starvation. After 4 hours of starvation, serially diluted C15Y (3-fold dilutions starting from a concentration of 10 nM), bispecific recombinant proteins LCB-020, LCB-021, LCB-023, and LCB-024 (3-fold dilutions starting from a concentration of 333 nM) were added, and the plate was incubated in a CO.sub.2 incubator at 37° C. for 72 hours. After 72 hours, the number of viable cells was detected with Celltiter-glo (Promega, Cat. #G7573).

    [0291] As shown in FIG. 25, the positive control C15Y exerts a very strong pro-proliferation effect at a very low concentration (EC50=0.05267 nM), while the bispecific recombinant protein of the present disclosure has to exert a pro-proliferation effect at a relatively high concentration (EC50 is about 21-37 nM), and there is no significant difference in EC50. Because M-07e do not express the target antigen of LCB-020, LCB-021, LCB-023 and LCB-024, M-07e can be regarded as a non-target cell of interest, and the bispecific recombinant protein of the present disclosure whose second functional binding fragment is IL15-IL15RαSUSHI may exert its pro-proliferation effect on non-target cells at a high concentration, the EC50 is over 400 times higher than that of the positive control.

    [0292] To sum up, it can be seen that, for the pro-proliferation effect of the bispecific recombinant protein of the present disclosure on the target cells of interest with positive antigen of interest, the pro-proliferation effect of the bispecific recombinant protein with targeting function is obviously stronger than that of the bispecific recombinant protein without targeting function, but is weaker than that of the positive control C15Y; on the contrary, the pro-proliferation effect of the recombinant protein of the present disclosure shows no significant difference on non-target cells of interest with negative antigen of interest, and the effective concentration of the pro-proliferation effect is significantly higher than that of the positive control C15Y. It can be seen that the bispecific recombinant protein of the present disclosure with targeting function may exert a pro-proliferation effect on target cells of interest at a relatively low concentration, but has to exert a pro-proliferation effect on non-target cells of interest at a very high concentration.

    Embodiment 14: Freeze-Thaw Stability Study of the Bispecific Recombinant Protein

    [0293] The existing recombinant human albumin interferon-α 2b fusion protein has poor freeze-thaw stability and is not suitable for repeated freezing and thawing. For example, PEGylated long-acting interferon should not be frozen and shaken, and has higher requirements for transportation and storage conditions. In order to study the freeze-thaw stability of the bispecific recombinant protein of the present disclosure, repeated freeze-thaw stability tests were performed on the bispecific recombinant protein. The protein was placed in 20 mM NaAc (PH=5) buffer and subjected to 5 repeated freeze-thaw cycles under the condition of −40° C. The purity (size exclusion chromatography, SEC) and appearance analyses were performed on samples before and after freeze-thaw. The results are shown in Table 5. LCB-011 and its mutants have good freeze-thaw stability, the purity is above 95%, and the appearance is clear after 5 repeated freeze-thaw cycles, indicating that the freeze-thaw stability of the IFN-α 2b protein part in the bispecific recombinant protein of the present disclosure is significantly better than that of IFN-α 2b monomer or PEGylated IFN-α 2b.

    TABLE-US-00005 TABLE 5 Freeze-thaw stability of bispecific recombinant proteins No freezing and thawing Freezing and thawing for 5 times SEC- Impurity with low Impurity with low Number HPLC(%) Monomer Multimer molecular weight Monomer Multimer molecular weight 1 LCB-011 96.50 3.50 ND 97.87 2.14 ND 2 LCB-011-M3 99.11 0.89 ND 97.68 2.32 ND 3 LCB-011-M4 98.03 1.97 ND 95.74 4.13 0.12

    [0294] The use of any and all embodiments or exemplary language (e.g., “such as”) provided herein is intended only to better illustrate the present disclosure, and does not pose a limitation on the scope of the present disclosure, unless otherwise required. No language in the specification should be construed as indicating any non-claimed element essential to the practice of the present disclosure.

    [0295] All publications and patent applications cited in this specification are incorporated herein by reference in their entireties to the same extent as if each individual publication or patent application is specifically and individually indicated to be incorporated by reference. Furthermore, any theory, mechanism, demonstration or finding described herein is intended to further enhance the understanding of the present disclosure, and is not intended to limit the present disclosure in any way to such theory, mechanism, demonstration or finding. While the present disclosure has been illustrated and described in detail in the drawings and foregoing description, such illustration and description should be regarded in an illustrative rather than a restrictive sense.

    [0296] Although the specific embodiments of the present disclosure have been described above, those skilled in the art should understand that these are only illustrative examples, and that various changes or modifications may be made to these embodiments without departing from the principle and essence of the present disclosure. Accordingly, the scope of protection of the present disclosure is defined by the appended claims.