Caspase Activator

1,3,5-Tricaffeoylquinic acid acts as an angiogenesis inhibitor and apoptosis inducer, and exhibits anti-HIV activity. 1,3,5-Tricaffeoylquinic acid inhibits the phosphorylation of VEGFR2, ERK, PI3K, Akt and mTOR in the angiogenesis signaling pathway. 1,3,5-Tricaffeoylquinic acid regulates apoptosis-related proteins, upregulates the levels of activated caspase-8, Bax, activated PARP and caspase-3/9, while downregulates the level of Bcl-2. 1,3,5-Tricaffeoylquinic acid inhibits tube formation and shows cytotoxicity against ovarian cancer cells. 1,3,5-Tricaffeoylquinic acid can be used in studies related to ovarian cancer.

AD-2646 (LCL102), a ceramide analog, can kill leukemic T cells (EC₅₀: 40 μM). AD-2646 triggers the cleavage of caspase-8, -9 and -3, as well as the caspase substrate PARP. AD-2646 is a ceramidase inhibitor. AD-2646 induces an accumulation of endogenous ceramide owing to perturbed ceramide metabolism.

Atiprimod (Azaspirane) hydrochloride is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML).

Alisol B acetate is a Triterpenoids product that can be isolated from the tubers of Alisma plantago-aquatica Linn..

AN-7 is an orally active histone deacetylase (HDAC) inhibitor that induces histone hyperacetylation and differentiation in vitro and in vivo, and inhibits the proliferation of human prostate 22Rv1 cancer cells. AN-7 can increase the expression of the pro-apoptotic protein Bax, reduce the expression of the anti-apoptotic protein Bcl-2, and promote apoptosis by activating caspase-3, and can be used in the study of prostate cancer.

Daphnoretin (Dephnoretin; Thymelol) (Standard) is the analytical standard of Daphnoretin (HY-N0699). This product is used for research and analytical applications. Daphnoretin is a protein kinase C (PKC) activator that can inhibit the expression of hepatitis B virus (HBV) surface antigen (HBsAg) and has antiviral activity. Daphnoretin exerts its anti-tumor effect by inhibiting the activation of the PI3K/AKT signaling pathway, triggering the mitochondrial apoptosis pathway. Daphnoretin alleviates chondrocyte apoptosis and inflammatory responses by inhibiting endoplasmic reticulum stress and the activation of the NLRP3 inflammasome. Daphnoretin can regulate the differentiation and maturation of dendritic cells, by down-regulating the phosphorylation level of JNK, inhibiting its immune stimulating function, thereby playing a protective role in skin transplant rejection reactions.

Perillyl alcohol (Standard) is the analytical standard of Perillyl alcohol (HY-N7000). Perillyl alcohol is an orally active monoterpene. Perillyl alcohol exhibits multiple activities such as analgesic, anti-inflammatory, anti-tumor, anti-angiogenic, and anti-nociceptive effects. Perillyl alcohol can induce apoptosis and cell cycle arrest in tumor cells.

Zenidolol (ICI-118551) (Standard) is the analytical standard of Zenidolol (HY-100543). This product is intended for research and analytical applications. Zenidolol is a selective β2-adrenergic receptor antagonist with K_i values of Zenidolol for β2, β1 and β3 adrenergic receptors of 0.7, 49.5 and 611 nM, respectively. Zenidolol exerts antitumor effects via inducing apoptosis, inhibiting tumor sphere formation, and downregulating the HIF pathway by blocking β2-AR on tumor cells. Zenidolol exhibits a unique pulmonary vessel-specific vasodilatory effect in mouse models. Zenidolol can be used as an intraocular pressure-lowering agent in ophthalmic disease research.

RKS262 is an orally active cyclin/CDK inhibitor. RKS262 is also an apoptosis inducer and cell cycle regulator, exhibiting cytotoxic activity against cancer cells. RKS262 induces caspase-3 cleavage, ROS generation, SAPK/JNK activation, and upregulates the expression of p53, Bid, Bad, Bok, and p27. RKS262 inhibits the expression of Bcl-2, Mcl-1, Bcl-xL, p21, cyclin D1, cyclin B1, cdc-2, cyclin D4, and DNA-pk KU-80 subunit. RKS262 suppresses the phosphorylation of the IGF-1R/PI3K/PKC pathway, ras oncogene activity, and Cdk-6, while increasing total Akt expression. RKS262 induces G₂/M or S phase cell cycle arrest, disrupts mitochondrial transmembrane potential, and reduces tumor burden in xenograft models. RKS262 is used in research on neuroblastoma and ovarian cancer.

EA-B2L is a GSTP degrader with a DC₅₀ of 48 μM in HeLa cells. EA-B2L inhibits GSTP enzymatic activity, induces dose-dependent GSTP degradation via the ubiquitin-proteasome and autophagy pathways, and does not activate the 20S proteasome subunit. EA-B2L induces dose-dependent apoptosis in cancer cells, a process associated with GSTP degradation, caspase 3 activation, and PARP cleavage. EA-B2L exerts dose-dependent antiproliferative effects on cancer cells with high GSTP expression. EA-B2L can be used in the research of cervical cancer, lung cancer, and fibrosarcoma.

FTI-277 TFA is a farnesyltransferase (FTase) inhibitor. FTI-277 TFA inhibits Ras farnesylation, blocks the phosphorylation of downstream ERK1/2 and mTOR, and reduces membrane-bound active N-ras protein. FTI-277 TFA activates caspase 3, upregulates Bim expression, induces cell apoptosis, suppresses regulatory T cell expansion, enhances macrophage phagocytosis, and improves bacterial clearance. FTI-277 TFA activates the PI3K/Akt signaling pathway, inhibits osteoblast differentiation, and reduces the proliferation ability of neuroblastoma cells. FTI-277 TFA can be used in research related to head and neck squamous cell carcinoma, neuroblastoma, sepsis, and vascular calcification.

3-Methylxanthine-d₃ is deuterated labeled 3-Methylxanthine (HY-50723). 3-Methylxanthine is a blood-brain barrier-permeable cyclic GMP phosphodiesterase inhibitor, with an IC₅₀ of 920 μM against guinea pig cyclic GMP phosphodiesterase. 3-Methylxanthine relaxes the spontaneous tension of isolated guinea pig tracheal smooth muscle preparations. Through a DRD1-dependent pathway, 3-Methylxanthine upregulates the expression of γH2AX and activated caspase-3, downregulates the expression of Bcl-2, and enhances Cisplatin-induced apoptosis (apoptosis) in ovarian cancer cells both in vitro and in vivo. 3-Methylxanthine induces clonic convulsions in the central nervous system. 3-Methylxanthine is the major metabolite of Theophylline (HY-B0809). 3-Methylxanthine can be used in studies related to ovarian cancer and neurotoxic convulsions.

IG-105 is an orally active and potent tubulin inhibitor that competitively inhibits [³H] colchicine binding to tubulin with an IC₅₀ of 0.6 μM and inhibits tubulin polymerization with an IC₅₀ of 3 μM. IG-105 inhibits microtubule polymerization by binding to the colchicine pocket of tubulin, induces G2-M phase arrest, and subsequently activates the caspase cascade through Bcl-2 inactivation and p53 upregulation, inducing apoptosis. IG-105 effectively overcomes multidrug resistance as a non-Pgp substrate. IG-105 can be used for research on leukemia, breast cancer, liver cancer, prostate cancer, lung cancer, melanoma, pancreatic cancer, and colon cancer.

Curcumenol (Standard) ((+)-Curcumenol (Standard)) is the analytical standard of Curcumenol (HY-N2259). This product is intended for research and analytical applications. Curcumenol ((+)-Curcumenol) is a natural compound with oral efficacy, exhibiting an IC₅₀ of 12.6 μM and a K_i of 10.8 μM against human CYP3A4. Curcumenol inhibits TNFα-induced phosphorylation/degradation of IκBα, phosphorylation/nuclear translocation of NF-κB p65, as well as the upregulation of MMP3, MMP9, MMP13, TRAF3, IL1RL1, TNFα and IL-1β. Curcumenol suppresses LPS-induced phosphorylation of Akt and p38 MAPK, as well as the production of pro-inflammatory mediators/proteins, and downregulates the SLC7A11/NF-κB/TGF-β pathway. Curcumenol binds to and inhibits the activation of Fyn and Lyn, blocks the function of downstream FcεRI signaling components, and reduces the release of allergic mediators/cytokines. Curcumenol upregulates the expression of KDM6B, and promotes chondrocyte proliferation and cartilage repair. Curcumenol induces ferroptosis and apoptosis, regulates the EMT process, and inhibits tumor growth and metastasis of triple-negative breast cancer. Curcumenol possesses anti-inflammatory, neuroprotective, antioxidant, antitumor, antiviral and hepatoprotective activities. Curcumenol can be used in research related to intervertebral disc degeneration, cancer, inflammation, central nervous system neurodegenerative diseases, allergic reactions and knee osteoarthritis.

Quinidine (15% dihydroquinidine) (Standard) is the analytical standard of Quinidine (15% dihydroquinidine) (HY-B1751). This product is intended for research and analytical applications. Quinidine (15% dihydroquinidine) is an orally active antiarrhythmic agent. Quinidine (15% dihydroquinidine) 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 (15% dihydroquinidine) exerts sustained block and open-channel block effects on I_K(f). Quinidine (15% dihydroquinidine) alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine (15% dihydroquinidine) can be used in studies related to uterine sarcoma and seizures.

Isomahanine, carbazole alkaloid, is an antioxidative agent. Isomahanine has DPPH radical scavenging activity with an IC₅₀ value of 24 μM.

USP7-IN-20 is a highly selective USP7 inhibitor that binds allosterically to the allosteric pocket of USP7 in a non-competitive and reversible manner. USP7-IN-20 downregulates MDM2 protein levels and stabilizes p53, thereby inducing p21 expression and enhancing the ubiquitin-dependent degradation of MDM2. USP7-IN-20 effectively binds endogenous USP7 to inhibit cancer cell proliferation, and also induces apoptosis by promoting the cleavage of PARP and caspase 3. USP7-IN-20 can be widely used in cancer-related basic and translational research.

Ibulocydine is an isobutyrate prodrug of the Cdk inhibitor BMK-Y101 (HY-188159), with oral activity, and exhibits IC₅₀ values of approximately 50 nM against CDK1/CDK2, 530 nM against CDK7/cyclin H/Mat1, and 85 nM against CDK9/cyclin T. Ibulocydine reduces the phosphorylation levels of Rb, nucleolin, and RNA polymerase II CTD Ser-5 and Ser-2, downregulates the expression of Mcl-1, survivin, and XIAP, decreases MMP-9 expression, and lowers the Bcl-2/Bax ratio, activates calpain-mediated Bax cleavage, cytochrome c release, and caspase activation. Ibulocydine induces apoptosis, inhibits the growth of cancer cells and xenografts, enhances the sensitivity of cancer cells to TRAIL and radiotherapy, and blocks cancer cell metastasis. Ibulocydine can be used in research related to various cancers, including hepatocellular carcinoma, triple-negative breast cancer, lung cancer, and colon cancer.

CDKi free base is a CDK inhibitor. CDKi free base induces morphological changes, DNA fragmentation, and cell death in vestibular schwannoma cells. CDKi free base downregulates pRb, EGF-R, PI3K, NF-κB, and Shh levels, while upregulating JNK, ASK1, Caspase 3, and p21, and induces PARP-1 cleavage. CDKi free base can be used in research related to vestibular schwannoma.

PETCM (Standard) is the analytical standard of PETCM (HY-103349). This product is intended for research and analytical applications. PETCM is an activator of caspase-3 and acts as an cytochrome c (cyto c)-dependent manner. PETCM promotes Apaf-1 oligomerization and induces cell apoptosis in HeLa cells.