kdm5

KDM5-C49 HCl (KDOAM-20 hydrochloride) is a potent and selective inhibitor of KDM5 demethylase. KDM5-C49 HCL(1596348-16-1 Free base) is a candidate compound for the treatment of cancer.

KDM5-C70 is an ethyl ester derivative of KDM5-C49 and functions as an effective, cell-permeable, pan-KDM5 histone demethylase inhibitor. It exhibits an antiproliferative effect in myeloma cells and induces a genome-wide elevation of H3K4me3 levels.

KDM5-C49 is a potent and selective inhibitor of KDM5, which regulates cell proliferation and stem cell self-renewal and differentiation.

KDM5-IN-1 is an effective and selective inhibitor of KDM5 with an IC50 of 15.1 nM.

KDM5-C49 (KDOAM-20) hydrochloride is a potent, selective inhibitor of the KDM5 family of demethylases, with IC50 values of 40 nM for KDM5A, 160 nM for KDM5B, and 100 nM for KDM5C. This compound is utilized in cancer research [1].

KDM5A-IN-1 is an orally available, potent and selective inhibitor of the pan-histidine lysine demethylase 5 KDM5, inhibiting KDM5A, KDM5B, and KDM5C with IC50 values of 45 nM, 56 nM, and 55 nM, respectively.KDM5A-IN-1 inhibits PC9 H3K4Me3, and may be useful in cancer research.

KDM5B-IN-3 (Compound 5) is an inhibitor of histone lysine-specific demethylase 5B (KDM5B) or JARID1B, with an IC50 value of 9.32 μM, and serves as a valuable tool in gastric cancer research [1].

Zavondemstat (QC8222 free base) is a histone lysine demethylase 4 (KDM4) inhibitor with anticancer and antitumor activity for the study of triple-negative and breast cancers.

KDM4-IN-2 is a potent and selective KDM4 KDM5 dual inhibitor with Kis of 4 and 7 nM for KDM4A and KDM5B, respectively.

CPI-455 is a specific KDM5 inhibitor.

CPI-455 analogue (CPI-455 analogue) is an analogue of CPI-455 which is a KDM5 inhibitor.

JQKD82 trihydrochloride, a cell-permeable and selective inhibitor of KDM5, enhances H3K4me3 levels and is utilized in multiple myeloma research.

KDOAM-25 trihydrochloride increases global H3K4 methylation at transcriptional start sites and impairs proliferation in multiple myeloma MM1S cells. KDOAM-25 trihydrochloride is a potent and highly selective histone lysine demethylases 5 (KDM5) inhibitor

KDOAM-25 citrate is a potent and highly selective histone lysine demethylases 5 (KDM5) inhibitor, with IC50 values of 71 nM, 19 nM, 69 nM, and 69 nM for KDM5A, KDM5B, KDM5C, and KDM5D, respectively. Multiple myeloma MM1S cells treated with KDOAM-25 citrate show increased global H3K4 methylation at transcriptional start sites and impaired proliferation [1].

KDOAM-25, a potent and highly selective inhibitor of histone lysine demethylases 5 (KDM5) with IC50 values of 71 nM for KDM5A, 19 nM for KDM5B, 69 nM for KDM5C, and 69 nM for KDM5D, enhances global H3K4 methylation at transcriptional start sites and reduces proliferation in multiple myeloma MM1S cells.

CPI-4203 is a selective inhibitor of KDM5 demethylases.

JQKD82 is a selective inhibitor of KDM5 and increases H3K4me3. JQKD82 can be used in studies about the treatment of multiple myeloma.

CPI-455 is a specific KDM5 inhibitor with IC50 value of 10 ± 1 nM for full-length KDM5A in enzymatic assays, elevating global levels of H3K4 trimethylation (H3K4me3) and decreased the number of DTPs in multiple cancer cell line models treated with target

JQKD82 (JADA82) dihydrochloride, a cell-permeable and selective inhibitor of KDM5, enhances H3K4me3 levels, making it effective for multiple myeloma research [1].

KDOAM-25 trihydrochloride is a potent and highly selective inhibitor of histone lysine demethylase 5 (KDM5), targeting KDM5A (IC50: 71 nM), KDM5B (IC50: 19 nM), KDM5C (IC50: 69 nM), and KDM5D (IC50: 69 nM). It enhances overall H3K4 methylation at the transcription start site and hinders the proliferation of multiple myeloma [MM1S cells].

TK-129 is an orally active, potent inhibitor of KDM5B with an IC50 of 44 nM and is low-toxicity. TK-129 exhibits cardioprotective effects by inhibiting KDM5B and blocking the KDM5B-associated Wnt pathway. TK-129 can be used in cardiovascular disease studies to reduce isoprenaline-induced myocardial remodelling and fibrosis in vivo, as well as to reduce ang II-induced activation of cardiac fibroblasts in vitro [1].

GSK467 is a potent and selective inhibitor of KDM5 (JARID1)(Ki : 10 nM).