C12Y114/11027

ENHANCING T-CELL FUNCTION AND TREATING A T-CELL DYSFUNCTIONAL DISORDER WITH A COMBINATION OF AN LSD INHIBITOR AND A PD-1 BINDING ANTAGONIST
20210186905 · 2021-06-24 ·

The present invention relates to a composition for enhancing T-cell function or for treating a T-cell dysfunctional disorder, the composition comprising, consisting or consisting essentially of a lysine specific demethylase (LSD) inhibitor (which may be a MAO inhibitor or phenelzine) and a Programmed cell death protein-1 (PD-1) binding antagonist (which may be an antibody, preferably nivolumab, pembrolizumab, lambrolizumab or pidilizumab).

Histone demethylase inhibitors

The present disclosure relates generally to compositions and methods for treating cancer and neoplastic disease. Provided herein are substituted pyridine derivative compounds, and compositions (including pharmaceutical compositions) that include these compounds. The subject compounds and compositions are useful for inhibition of at least one histone demethylase. Furthermore, the subject compounds and compositions are useful for the treatment of cancer or neoplastic disease, such as prostate cancer, breast cancer, bladder cancer, lung cancer, melanoma, retinoblastoma, or multiple endocrine neoplasia type 1.

METHODS AND COMPOSITIONS TO INCREASE HUMAN SOMATIC CELL NUCLEAR TRANSFER (SCNT) EFFICIENCY BY REMOVING HISTONE H3-LYSINE TRIMETHYLATION, AND DERIVATION OF HUMAN NT-ESC
20200181648 · 2020-06-11 ·

The present invention provides methods and compositions to improve the efficiency of somatic cell nuclear transfer (SCNT) of human cells and the consequent production of human nuclear transfer ESC (hNT-ESCs). More specifically, the present invention relates to the discovery that trimethylation of Histone H3-Lysine 9 (H3K9me3) in reprogramming resistant regions (RRRs) in the nuclear genetic material of human donor somatic cells prevents efficient human somatic cell nuclear reprogramming or SCNT. The present invention provide methods and compositions to decrease H3K9me3 in methods to improve efficacy of hSCNT by exogenous or overexpression of the demethylase KDM4 family and/or inhibiting methylation of H3K9me3 by inhibiting the histone methyltransferases SUV39h1 and/or SUV39h2.

HISTONE DEMETHYLASE INHIBITORS

The present disclosure relates generally to compositions and methods for treating cancer and neoplastic disease. Provided herein are substituted pyridine derivative compounds, and compositions (including pharmaceutical compositions) that include these compounds. The subject compounds and compositions are useful for inhibition of at least one histone demethylase. Furthermore, the subject compounds and compositions are useful for the treatment of cancer or neoplastic disease, such as prostate cancer, breast cancer, bladder cancer, lung cancer, melanoma, retinoblastoma, or multiple endocrine neoplasia type 1.

Histone demethylase inhibitors

The present disclosure relates generally to compositions and methods for treating cancer and neoplastic disease. Provided herein are substituted pyridine derivative compounds, and compositions (including pharmaceutical compositions) that include these compounds. The subject compounds and compositions are useful for inhibition of at least one histone demethylase. Furthermore, the subject compounds and compositions are useful for the treatment of cancer or neoplastic disease, such as prostate cancer, breast cancer, bladder cancer, lung cancer, melanoma, retinoblastoma, or multiple endocrine neoplasia type 1.

APPLICATION OF UTX GENE IN PREPARATION OF DRUGS FOR PREVENTING OR TREATING LIPID DISEASES
20200024580 · 2020-01-23 ·

An application of a UTX gene in preparation of drugs for preventing or treating lipid diseases. The invention further discloses a method for knocking out a UTX gene from a mouse liver. The invention further discloses a UTX overexpression adenovirus as well as a preparation method and an application thereof. The invention further discloses a method for upregulating UTX expression in a mouse liver. The invention further discloses therapeutic action of UTX overexpression on HFD induced hyperlipidemia and NAFLD. The invention provides an available laboratory basis for preparing lipid-lowering drugs, so that the UTX can be used for preparing drugs affecting the lipid, and a new research method is provided for researching the occurrence and development of dyslipidemia.

REPROGRAMMING CELL AGING

Disclosed herein are methods and compositions for identifying transcriptional and epigenetic age-related markers. Disclosed herein are also methods and compositions for reprogramming cell age by modulating transcriptional and epigenetic age-related markers identified herein. The identified transcriptional and epigenetic age-related markers can also be used for measuring cellular age in a cell or tissue.

INDUCIBLE SINGLE AAV SYSTEM AND USES THEREOF
20240123086 · 2024-04-18 · ·

Aspects of the disclosure relate to compositions and methods for epigenetic regulation of endogenous gene expression from viral vectors. In some embodiments, the disclosure provides expression constructs comprising a viral vector encoding a transgene, the activation of which is regulated by a rapamycin/rapalog-based system, and the transgene is capable of epigenetically regulate an endogenous gene.

HISTONE DEMETHYLASE INHIBITORS

The present disclosure relates generally to compositions and methods for treating cancer and neoplastic disease. Provided herein are substituted pyridine derivative compounds, and compositions (including pharmaceutical compositions) that include these compounds. The subject compounds and compositions are useful for inhibition of at least one histone demethylase. Furthermore, the subject compounds and compositions are useful for the treatment of cancer or neoplastic disease, such as prostate cancer, breast cancer, bladder cancer, lung cancer, melanoma, retinoblastoma, or multiple endocrine neoplasia type 1.

METHODS AND COMPOSITIONS TO INCREASE HUMAN SOMATIC CELL NUCLEAR TRANSFER (SCNT) EFFICIENCY BY REMOVING HISTONE H3-LYSINE TRIMETHYLATION, AND DERIVATION OF HUMAN NT-ESC

The present invention provides methods and compositions to improve the efficiency of somatic cell nuclear transfer (SCNT) of human cells and the consequent production of human nuclear transfer ESC (hNT-ESCs). More specifically, the present invention relates to the discovery that trimethylation of Histone H3-Lysine 9 (H3K9me3) in reprogramming resistant regions (RRRs) in the nuclear genetic material of human donor somatic cells prevents efficient human somatic cell nuclear reprogramming or SCNT. The present invention provide methods and compositions to decrease H3K9me3 in methods to improve efficacy of hSCNT by exogenous or overexpression of the demethylase KDM4 family and/or inhibiting methylation of H3K9me3 by inhibiting the histone methyltransferases SUV39h1 and/or SUV39h2.