cleaved-parp

CSRM617 hydrochloride is a selective small-molecule inhibitor of the transcription factor ONECUT2 (OC2, a master regulator of androgen receptor), with a Kd of 7.43 µM in SPR assays, directly binding to the OC2-HOX domain. CSRM617 hydrochloride induces apoptosis through the appearance of cleaved Caspase-3 and PARP and is well tolerated in the mouse model of prostate cancer [1].

Emamectin Benzoate (MK-244), by binding gamma-aminobutyric acid (GABA) receptor and glutamate-gated chloride channels disrupting nerve signals within arthropods, acts as a chloride channel activator.

FGFR-IN-13 (compound III-30), an irreversible covalent inhibitor of the fibroblast growth factor receptor (FGFR), effectively modulates signaling through FGFR1 (IC 50 = 0.20 ± 0.02 nM) and FGFR4 (IC 50 = 0.40 ± 0.03 nM). It suppresses the expression of crucial proteins such as total-PARP and Bcl-2, while enhancing the expression of Cleaved-PARP and Bax in a dose-dependent manner. Notably, FGFR-IN-13 demonstrates considerable antitumor and oral activity [1].

RPS6-IN-1 (Compound 22o) inhibits cell migration and induces apoptosis (increasing the expression of Bax, p53, cleaved-caspase 3, and cleaved-PARP). It reduces mitochondrial membrane potential and activates autophagy (Autophagy) through the PI3K-Akt-mTOR signaling pathway, damaging mitochondria and lysosomes within the cell and causing endoplasmic reticulum stress. RPS6-IN-1 also inhibits the phosphorylation of RPS6. Notably, RPS6-IN-1 is a low systemic toxicity anticancer agent.

JNJ-1013 is a potent and selective IRAK1 degrader, with IC50 values of 72 nM for IRAK1, 443 nM for IRAK4, and 1071 nM for VHL FP. It induces apoptosis, increases cleaved PARP expression, and decreases the expression of IRAK1, p-IKBα, and pSTAT3(Tyr705) [1].

Anticancer agent 71 (Compound 4b) is a potent anticancer agent that arrests the cell cycle at the G2 M phase and induces apoptosis by upregulating Bax, Ikb-α, and cleaved PARP, while downregulating Bcl-2 expression levels.

Anticancer agent 137 (8q), a potent PI3k inhibitor, exhibits broad-spectrum anticancer activity by inducing G2/M cell cycle arrest and apoptosis. It increases levels of cleaved PARP, and caspases 3 and 7, making it useful in cancer research [1].