cleaved-parp

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.

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].

EV206 is a potent Hsp70 inhibitor, demonstrating significant anti-proliferative activity. This compound induces apoptosis and promotes increased protein expression of cleaved PARP and caspase-3, indicating its potential anti-tumor activity.

MAPK-IN-3 (Compound 4a) is an antiproliferative agent demonstrating significant inhibitory effects on KYSE 30, HCT 116, and HGC 27 cell lines, with IC50 values of 0.57 μM, 3.27 μM, and 2.28 μM, respectively. This compound arrests the cell cycle via a p53-dependent mechanism and induces apoptosis through a p53-independent pathway. It reduces the expression of cell cycle-related proteins, such as Cyclin D1 and Cyclin B1, while increasing pro-apoptotic proteins like cleaved PARP, cleaved caspase-7, and cleaved caspase-9. MAPK-IN-3 also decreases anti-apoptotic proteins such as Bcl-2, elevates ROS levels in KYSE 30 cells, and enhances the expression of ROS-related MAPK pathway members, including p-ERK, p-p38, and p-JNK.

STING-IN-17 is an orally active inhibitor of STING (human STING IC50= 29 nM, murine STING IC50= 15 nM). It effectively suppresses the phosphorylation of STING, TBK1, and IRF3. The compound inhibits the expression of IP10, IFNB1, and ISG56 mRNA in a dose-dependent manner. Additionally, STING-IN-17 reduces ROS and inhibits the expression of cleaved-PARP/caspase-3. It shows potential for improving renal function and can be utilized in research on inflammatory diseases such as acute kidney injury.

Sino-C is a Sinomenine derivative with anticancer properties. It disrupts cholesterol homeostasis by upregulating crucial genes such as SREBF2 and HMGCS1, leading to intracellular cholesterol accumulation and lipid droplet formation. The metabolic disturbance induced by Sino-C further triggers lipid peroxidation and endoplasmic reticulum (ER) stress, initiating a unique mixed form of cell death that includes both apoptotic (cleaved PARP) and necrotic-like features. Sino-C is applicable in studies of colorectal cancer, lung cancer, and breast cancer.

dCDK9-202 is a potent CDK9-PROTAC degrader with a DC50 value of 3.5 nM. It exhibits broad-spectrum antitumor activity and significantly disrupts oncogenic transcriptomes. dCDK9-202 activates Caspase-3/7, increases levels of cleaved PARP, and directly induces tumor cell apoptosis (apoptosis). It effectively inhibits the growth of TC-71 tumors without any observed toxicity in mice. dCDK9-202 is applicable for researching EGFR-driven cancers, such as sarcomas.

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.

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 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].

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.