Caspase Activator

EMT inhibitor-3 (compound 11i) is a epithelial-mesenchymal transition (EMT) inhibitor. EMT inhibitor-3 inhibits neuroblastoma SK-N-SH cells with an IC₅₀ of 2.5 μM. EMT inhibitor-3 inhibits SK-N-SH cell proliferation, migration, and invasion. EMT inhibitor-3 increases the Bax/Bcl-2 protein expression ratio, promotes Cytochrome C ( HY-125857) release from mitochondria, and activates caspases 9 and caspases 3, inducing mitochondria-mediated endogenous tumor cell Apoptosis. EMT inhibitor-3 is potential for cancer research.

Apoptotic agent-2 (compound 14b) induces apoptosis by down-regulation of Bcl-2 and up-regulation of Bax and caspase-3. Apoptotic agent-2 exhibits anti-proliferative activities and can be used for cancer research.

N1,N11-Diethylnorspermine is a synthetic analog of the naturally occurring polyamine spermine, can induce polyamine depletion and inhibit tumor cell growth. N1,N11-Diethylnorspermine activates polyamine catabolism and downregulates mTOR protein. N1,N11-Diethylnorspermine induces the release of cytochrome c from mitochondria, resulting in activation of caspase 3. N1,N11-Diethylnorspermine tetrahydrochloride kills glioblastoma multiforme (GBM) through induction of SSAT (spermidine/spermine N1-acetyltransferase) coupled with H₂O₂ production.

DdBIC is a pyroptosis inducer. DdBIC binds to Nur77 and triggers its translocation to mitochondria, activates SDHA to deplete succinyl-CoA, disrupts heme homeostasis, induces electron leakage, and elicits mitochondrial ROS production. DdBIC induces mitochondrial ROS that oxidatively activates OMA1, promotes OPA1 cleavage and its release into the cytoplasm, activates the integrated stress response via PERK, and ultimately activates granzyme B to cleave GSDMC. DdBIC can be used for the study of melanoma.

ST09 is an efficient and low toxicity Curcumin (HY-N0005) derivative. ST09 significantly inhibits cell migration and downregulates the expression of MMP1, MMP2, and Vimentin. ST09 has strong cytotoxicity to breast cancer cells, such as MDA-MB-231, MCF7 and T47D cells. ST09 induces cell apoptosis by upregulating Bax and cleaved caspase-3/9. ST09 can be used in the research of cancer such as breast cancer.

Quinidine sulfate is an orally active antiarrhythmic agent. Quinidine sulfate reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine sulfate exerts sustained block and open-channel block effects on I_K(f). Quinidine sulfate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine sulfate can be used in studies related to uterine sarcoma and seizures.

FS102 is a selective Fc fragment with antigen binding (Fcab) that targets HER2 with a K_D value of 0.8 nM. FS102 induces the degradation of HER2, activates Caspase 3/7 and disrupts the integrity of the cell membrane, triggering apoptosis of tumor cells. FS102 is promising for research of cancers such as breast cancer, gastric cancer, and colorectal cancer.

Caspase-3/7 activator 1 is an effective activator of Caspase-3/7. Caspase-3/7 activator 1 has tumor selectivity, anti-proliferative activity and high Apoptosis-inducing ability.

HDAC-IN-99 is a histone deacetylase (HDAC) inhibitor with an IC₅₀ of 37.73 nM, and it exhibits potent inhibitory activity against HDAC1 (IC₅₀ = 48.09 nM), HDAC2 (IC₅₀ = 300.28 nM) and HDAC6 (IC₅₀ = 9.16 nM). HDAC-IN-99 exerts broad-spectrum antiproliferative activity in various cancer cell lines. HDAC-IN-99 induces S-phase cell cycle arrest and apoptosis in colon cancer cells, increases the acetylation levels of histone H3, histone H4 and α-tubulin, and upregulates the expression of p21 as well as the cleavage of caspase-3. HDAC-IN-99 displays antitumor activity in colon cancer xenograft models. HDAC-IN-99 can be used for the research of colon cancer.

d-(KLAKLAK)₂, Proapoptotic Peptide acetate is a pro-Apoptotic peptide whose core mechanism of action is to disrupt organelle membranes, especially mitochondrial membranes, thereby inducing apoptosis. d-(KLAKLAK)₂, Proapoptotic Peptide acetate activates the activity of caspase 3/7 in cancer cells. Although d-(KLAKLAK)₂ Proapoptotic Peptide acetate exhibits very low toxicity to eukaryotic cells extracellularly, it cannot effectively penetrate cell membranes to enter the cytoplasm on its own. d-(KLAKLAK)₂, Proapoptotic Peptide acetate must be conjugated with a carrier capable of "homing" and "internalization" to exert its anti-cancer effects.

PROTAC BRD4 Degrader-6 (compound 32a) is a potent small-molecule BRD4PROTAC degrader with IC₅₀ value of 2.7 nM for BRD4 BD1. PROTAC BRD4 Degrader-6 potently degrades BRD4 protein and inhibits the expression of c-Myc. PROTAC BRD4 Degrader-6 inhibits the proliferation of pancreatic cancer cell line BxPC3 and induces apoptosis. PROTAC BRD4 Degrader-6 can be used for human pancreatic cancer research.

HDAC-IN-100 is a histone deacetylase inhibitor with an IC₅₀ of 0.038 μM against HDAC1, 0.283 μM against HDAC2, and 0.586 μM against HDAC3. HDAC-IN-100 acts as a chemosensitizer and apoptosis inducer, activates caspase 3/7, and reverses Cisplatin (HY-17394) resistance. HDAC-IN-100 exerts antiproliferative effects in ovarian cancer cells and squamous cancer cells. HDAC-IN-100 is applicable for research related to ovarian cancer, squamous cell carcinoma, and Cisplatin (HY-17394)-resistant squamous cell carcinoma.

Ly101-4B is an apoptosis inducer and multi-target inhibitor with antiproliferative, antitumor and cycytotoxic effects. Ly101-4B reduces HSF1 expression, inhibits microRNA-214 synthesis, downregulates HSP27, HSP70 and HSP90 expression, while suppressing E2F-dependent transcriptional activity and downregulating its target genes. Ly101-4B induces caspase 3/7-mediated apoptosis by reducing DNA synthesis, inhibiting the cell cycle and G1/S phase transition, without affecting RNA synthesis or inducing necrosis. Ly101-4B is selective for pancreatic ductal adenocarcinoma cells with different genotypes and varying degrees of E2F dependence. Ly101-4B can be used in research related to epithelial ovarian cancer and pancreatic ductal adenocarcinoma.

AKT1-IN-13 is an orally active AKT1 inhibitor with an IC₅₀ of 5.17 μM. AKT1-IN-13 also exhibits high inhibitory activity against PAK1, PKA, MAP2K1 (MEK1 / MAPKK1) and MAPK1 (ERK2). AKT1-IN-13 induces cell apoptosis, activates the pro-apoptotic protein BAX, inhibits the anti-apoptotic protein Bcl-2, and activates caspase 3 simultaneously. As a cytotoxic agent, AKT1-IN-13 exerts a killing effect on orthotopically transplanted liver cancer in an AKT1-dependent manner. AKT1-IN-13 can be used in studies related to hepatocellular carcinoma.

Antitumor agent-72 (compound 6w) is a potent anticancer agent. Antitumor agent-72 has anticancer activity and induces apoptosis through activation of caspase-3 and cleavage of PARP. Antitumor agent-72 can be used for cancer research.

TPP-C8-CO-DSG bromide is a derivative of Diosgenin (HY-N0177) and an anticancer agent. TPP-C8-CO-DSG bromide downregulates Bcl-2 expression and upregulates Bax expression. TPP-C8-CO-DSG bromide promotes the cleavage of Caspase 9, Caspase 3 and PARP-1. TPP-C8-CO-DSG bromide depolarizes mitochondrial membrane potential, reduces intracellular ATP production, and induces intracellular ROS accumulation. TPP-C8-CO-DSG bromide promotes Apoptosis. TPP-C8-CO-DSG bromide exhibits anticancer activity against prostate cancer, breast cancer, lung adenocarcinoma, cervical cancer and colorectal cancer. TPP-C8-CO-DSG bromide can be used in the research of cervical cancer.

ADP-β-S (Adenosine 5'-(β-thiodiphosphate)) is a non-hydrolyzable ADP analog and a P2Y12 receptor agonist. ADP-β-S activates the P2Y12 receptor in microglia, thereby triggering downstream inflammatory signaling pathways. ADP-β-S activates P2Y purinergic receptors in rat pancreatic β cells and enhances glucose-induced insulin secretion. ADP-β-S can be used in the research of diseases such as inflammation and diabetes.

Estrogen receptor modulator 10 (compound G-5b) is an estrogen receptor (ER) antagonist (IC₅₀=6.7 nM) and degrader (DC₅₀=0.4 nM). Estrogen receptor modulator 10 is developed based on the Fulvestrant (HY-13636) molecule and can rapidly degrade ER receptors through the proteasome pathway. Estrogen receptor modulator 10 can induce cell apoptosis and block cells in the G1/G0 phase and can be used in cancer research.

HDSI-18 is an orally active HDAC6 selective inhibitor (IC₅₀: 1.6 nM). HDSI-18 is cytotoxic to K562, MV4-11, MOLM-13, THP-1, and Jurkat cells (IC₅₀: 0.48, 0.58, 0.91, 1.79, and 4.31 μM, respectively). HDSI-18 activates Caspase-3, induces mitochondrial depolarization and apoptosis, and has antitumor activity.

IDO1-IN-34 is a selective IDO1 inhibitor with an IC₅₀ of 0.093 μM. IDO1-IN-34 exhibits cytotoxicity against various cancer cell lines. IDO1-IN-34 inhibits the kynurenine (kynurenine) pathway and activates IL-2. IDO1-IN-34 induces cell apoptosis via the endogenous mitochondrial pathway, while increasing the levels of cytochrome c, caspase-3, caspase-9 and PARP-1. IDO1-IN-34 can be used for research on liver cancer, lung cancer, breast cancer, prostate cancer, colon cancer and leukemia.