Degradation compounds include a cyclic cell penetrating peptide (cCPP) and a degradation construct. The degradation construct includes a degradation moiety and a targeting moiety. The targeting moiety binds a target protein. When the targeting moiety is bound to the target protein, the degradation moiety mediates degradation of the target protein. The cCPP facilitates transfer of the degradation construct into a cell. The degradation compound may further include an exocyclic peptide to enhance endosomal escape of the compound or degradation construct once inside the cell.

The present invention relates to inhibitors of HERV proteins comprising HERV Env and/or Gag, or fragments thereof, for use in treating a tauopathy, Parkinson's disease, or ALS (Amyothrophic Lateral Sclerosis). The present invention further relates to inhibitors of receptors which bind HERV Env proteins for use in treating a tauopathy, Parkinson's disease, or ALS (Amyothrophic Lateral Sclerosis). The present invention further relates to molecules binding to HERV Env and/or Gag, or fragments thereof, or to a nucleic acid molecule encoding said HERV Env and/or Gag, or fragments thereof, for use in diagnosing a tauopathy, Parkinson's disease, or ALS.

The present disclosure relates to an endogenous Retrovirus K protein (ERVK) with an alternative envelope protein titled CTXLP. Said CTXLP peptide is represented by the sequences set forth in SEQ ID NO: 1. Additionally, antibodies that specifically recognize the epitope(s) set forth in SEQ ID NO:1 are and methods of use thereof and kits comprising the peptide set forth in SEQ ID NO:1 are also included in the present disclosure.

The present invention deals with innovative compounds and compositions for preventing and/or treating a newly discovered detrimental mechanism, which blocks the endogenous myelin repair capacity of the adult nervous system (NS) in diseases associated with the expression of HERV-W envelope protein (ENV), in particular of its MSRV subtype.

The present invention relates to methods and kits for diagnosis of cancer in a subject by detecting human endogenous retrovirus env (HERV-WL) polypeptides.

Methods for viral clearance using low pH hold based on a statistical design of experiment are provided. Several factors are evaluated to characterize the impacts of a low pH hold step for virus inactivation, including the factors of pH conditions, conductivity conditions, protein type, temperature, acid titrant, spike timing, and post-spike filtration. In addition to the effect of pH on virus inactivation, an increase in ionic strength through manipulating the conductivity can be a key component that influences virus inactivation kinetics.

Provided are recombinant adeno-associated virus (rAAV) compositions for the expression of antibodies (e.g., anti-complement component 5 (C5) antibodies) in cells, and methods of treating disorders with the same (e.g., disorders associated with C5 activity (e.g., Paroxysmal Nocturnal Hemoglobinuria)). Also provided are compositions, systems and methods for making the rAAV compositions.

Described herein are interleukin-10 receptor-2 peptides, antibodies that bind the peptides, compositions including the peptides and antibodies and methods of use of the peptides and antibodies. The interleukin-10 receptor-2 peptide consists of an 8-15 amino acid sequence that includes SEQ ID NO: 1 ((I/V)P(P/K/V/E)P(E/K/R/Q)N(A/V)R), SEQ ID NO: 2 ((S/L/V)PAF(A/P)(K/Q)(G/T/E)(N/T/D)), or SEQ ID NO: 3 (PP(G/T/Q/V)(V/T/A)(R/H/T/S)(GN/NHP/SAA)).

The present invention relates to a novel antibody against HERV-K envelope that targets a conserved region not affected by glycosylation or by native conformation, and its use in diagnostics and/or is therapy.

The present invention features anti-HERV-K monoclonal antibodies or antigen-binding portions thereof. The present invention also features uses of the antibodies for treating HIV infection or HIV-associated conditions or diseases.