PARP Activator

7-Epi 10-desacetyl paclitaxel (Standard) (7-epi-10-deacetyltaxol (Standard); 10-Deacetyl-7-epipaclitaxel (Standard)) is the analytical standard of 7-Epi 10-desacetyl paclitaxel (HY-77572). This product is intended for research and analytical applications. 7-Epi 10-desacetyl paclitaxel (7-epi-10-deacetyltaxol; 10-Deacetyl-7-epipaclitaxel) is a taxane diterpenoid that can be found in Taxus species and is also produced by the endophytic fungus Pestalotiopsis microspora. 7-Epi 10-desacetyl paclitaxel inhibits cancer cell proliferation and induces apoptosis and cell cycle arrest. 7-Epi 10-desacetyl paclitaxel induces apoptosis through the intrinsic mitochondrial pathway, a process associated with ROS generation, an increased Bax/Bcl-2 ratio, and PARP cleavage. 7-Epi 10-desacetyl paclitaxel can be used in research on hepatocellular carcinoma.

Desethylamiodarone (N-Desethylamiodarone; LB 33020) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone can be used in cervical cancer-related research.

HL435 is a BRD4 PROTAC degrader with DC₅₀ values of 11.9 nM (MDA-MB-231 cells) and 21.9 nM (MCF-7 cells), respectively. HL435 recruits the CRL4_DCAF11 E3 ubiquitin ligase complex to degrade BRD4 via the ubiquitin-proteasome system. HL435 induces cell cycle arrest and apoptosis (apoptosis) in cancer cells, downregulates the expression levels of cyclin D1 and cyclin B1, activates caspase-9, and induces PARP1 cleavage. HL435 exerts anti-tumor activity both in vitro and in mouse xenograft tumor models. HL435 can be used for the research of breast cancer and prostate 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.

CM002 is a circadian clock activator. CM002 inhibits the lineage commitment and terminal differentiation of preadipocytes by activating the circadian clock, thereby blocking the adipogenesis process driven by Wnt signaling-mediated transcriptional induction. CM002 attenuates lipid storage in a clock-dependent manner via inhibition of the lipogenic program in mature adipocytes. CM002 enhances circadian clock output across various adipose depots in both lean and obese mice through BMAL1/CLOCK-dependent metabolic reprogramming, inhibits adipocyte development and hypertrophy, and improves insulin sensitivity. CM002 can be used in research on obesity and type 2 diabetes.

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.

KB-15 is a STAT3 inhibitor. KB-15 exhibits potent anti-proliferative activity against AGS gastric cancer cells (IC₅₀ = 0.29 μM) and BGC-823 gastric cancer cells (IC₅₀ = 0.65 μM). KB-15 exerts anti-tumor effects by inhibiting STAT3 phosphorylation, downregulating HO-1 expression, and promoting intracellular ROS accumulation. KB-15 induces G0/G1 phase cell cycle arrest and apoptosis, as well as suppresses colony formation and migration of gastric cancer cells. KB-15 demonstrates excellent anti-tumor efficacy in BGC-823 subcutaneous xenograft model. KB-15 can be used for the study of gastric cancer.

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.

Quinidine polygalacturonate is an orally active antiarrhythmic agent. Quinidine polygalacturonate 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 polygalacturonate exerts sustained block and open-channel block effects on I_K(f). Quinidine polygalacturonate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine polygalacturonate can be used in studies related to uterine sarcoma and seizures.

LWY713 is a FLT3 PROTAC degrader with a DC₅₀ of 0.64 nM. LWY713 selectively induces FLT3 degradation in a cereblon- and proteasome-dependent manner. LWY713 induces G0/G1 cell cycle arrest and triggers apoptosis. LWY713 upregulates PARP and cleaved caspase 3, and inhibits the phosphorylation of FLT3, STAT5, AKT and Erk. LWY713 exhibits antitumor activity in xenograft mouse models. LWY713 can be used for the research of acute myeloid leukemia.

Cyproheptadine hydrochloride (Standard) (Cyproheptadine HCl (Standard)) is the analytical standard of Cyproheptadine hydrochloride (HY-B0366A). This product is intended for research and analytical applications. Cyproheptadine hydrochloride (Cyproheptadine HCl) acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine hydrochloride mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine hydrochloride induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine hydrochloride inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine hydrochloride can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia.

PROTAC EZH2 Degrader-44 (compound 60) is a highly efficient PROTAC degrader targeting the EZH2-PRC2 complex. By recruiting the CRBN E3 ligase and relying on the proteasome system, PROTAC EZH2 Degrader-44 simultaneously induces the degradation of core components EZH2, SUZ12 and EED, thereby significantly reducing the levels of H3K27me3 and CARM1. PROTAC EZH2 Degrader-44 exerts antiproliferative effects through a dual mechanism: on the one hand, it triggers mitochondrial dysfunction leading to decreased membrane potential; on the other hand, it strongly promotes apoptosis by regulating Bcl-2 family proteins (upregulating Bax, Caspase-3 and PARP, and downregulating Bcl-2). PROTAC EZH2 Degrader-44 exhibits only extremely low cytotoxicity in human normal mammary epithelial, liver and kidney cells, showing a favorable safety window. PROTAC EZH2 Degrader-44 is an ideal tool molecule for exploring the mechanisms of targeted therapy for triple-negative breast cancer.

Desethylamiodarone-d₄ hydrochloride (N-Desethylamiodarone-d₄ hydrochloride; LB 33020-d₄ hydrochloride) is the deuterated-labeled Desethylamiodarone hydrochloride (HY-130353). Desethylamiodarone hydrochloride (N-Desethylamiodarone hydrochloride; LB 33020 hydrochloride) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone hydrochloride downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone hydrochloride can be used in cervical cancer-related research.

PROTAC BET Degrader-15 is a BET PROTAC degrader with DC₅₀ values of <0.10 nM, <0.01 nM, and <0.01 nM against BRD2, BRD3, and BRD4, respectively. PROTAC BET Degrader-15 induces significant G2/M phase cell cycle arrest and triggers apoptosis. PROTAC BET Degrader-15 causes marked downregulation of c-Myc, accompanied by upregulation of the cell cycle inhibitory protein p21, downregulation of CDK6, and an increase in the apoptosis marker cleaved PARP. PROTAC BET Degrader-15 is applicable to the research of hematologic malignancies and lung cancer.

Lss-11 is a topoisomerase inhibitor. LSS-11 enhances cell death in cancer cells by inducing apoptosis through increasing the DR5 protein level and PARP1 cleavage. LSS-11 dose-dependently reduces STAT3 phosphorylation, downregulates its target genes MDR1 and MRP1, reduces P-gp protein expressionwithout affecting P-gp transport function. Lss-11 is a chemosensitizer and shows synergistic anticancer effect with Paclitaxel (HY-B0015). Lss-11 can be used for the research of paclitaxel-resistant lung cancer.

Pan-PDK degrader-1 is a pan-PDK class PROTAC degrader that degrades PDK2, PDK3 and PDK4 with DC₅₀ values of 9.2 nM, 9.9 nM and 11.5 nM, respectively. Pan-PDK degrader-1 recruits the mitochondrial protease HsClpP and induces selective pan-PDK degradation via HsClpP-mediated proteolysis. Pan-PDK degrader-1 reprograms mitochondrial metabolism toward oxidative phosphorylation, promoting ROS accumulation, mitochondrial permeability transition pore opening, endogenous mitochondrial apoptosis, calreticulin exposure and HMGB1 release. Pan-PDK degrader-1 upregulates cleaved Caspase-9, Caspase-3 and PARP. Pan-PDK degrader-1 inhibits primary and distal tumor growth via selective degradation of PDK in tumor tissues. Pan-PDK degrader-1 can be used for the research of breast cancer.

IHMT-BMX-068 is a BMX PROTAC degrader with a DC₅₀ of 0.007 μM. IHMT-BMX-068 promotes ubiquitination and degradation of BMX. IHMT-BMX-068 increases the levels of cleaved PARP and cleaved Caspase-3, and induces Apoptosis. IHMT-BMX-068 exerts anti-cancer effects against prostate cancer. IHMT-BMX-068 can be used for the research of prostate cancer.

Proadifen (hydrochloride) (Standard) is the analytical standard of Proadifen (hydrochloride). This product is intended for research and analytical applications. Proadifen (SKF-525A) hydrochloride is a non-competitive Cytochrome P450 inhibitor with an IC50 value of 19 μM. Proadifen hydrochloride reduces monoamine oxidase A (MAO-A) activity and reverses the antidepressantlike behavioral effect of Imipramine (HY-B1490A) and Desipramine (HY-B1272A) in rats. Proadifen hydrochloride also reduces N, N-dimethyltryptamine (DMT) metabolism in liver microsomes and inhibits N-demethylationand Acridone (HY-W007771) formation. Proadifen hydrochloride augments Lipopolysaccharide (LPS) (HY-D1056)-induced fever and exacerbates Prostaglandin E2 (PGE2) (HY-101952) levels in the rat. Proadifen hydrochloride is promising for research of metabolism-related deseases, ovarian carcinoma, inflammation and dopamine neurons-related deseases[4].

PROTAC MLKL Degrader-3 is a MLKL PROTAC degrader with DC₅₀ values of 248.9 nM (Hepa1-6) and 271.3 nM (HepG2), respectively. PROTAC MLKL Degrader-3 induces proteasome- and cereblon-dependent MLKL degradation via ubiquitination. PROTAC MLKL Degrader-3 reduces intratumoral MLKL levels and inhibits tumor growth in mice. PROTAC MLKL Degrader-3 can be used in the research of hepatocellular carcinoma.

Longilactone is a quassinoid diterpenoid isolated from the roots of Eurycoma longifolia. Longilactone induces apoptosis in MCF-7 cells via the extrinsic caspase pathway, activating the cleavage of caspase-8, caspase-7 and PARP. Longilactone can be used in research related to breast cancer and human lung cancer.