Bcl-2 Family Modulator

MAHS-3 is a thymidylate synthase (TS) and dihydrofolate reductase (DHFR) inhibitor, with IC₅₀ values of 5.279 μM and 52.60 μM against human targets, respectively. MAHS-3 exhibits broad-spectrum antiproliferative activity against cancer cells, induces cell cycle arrest, activates endogenous caspase-dependent apoptosis, reduces MMP levels, inhibits cell migration, increases intracellular NO levels, and promotes autophagy activity. MAHS-3 can be used in cancer-related research.

XSJ151 is a topoisomerase I inhibitor, stabilizing the DNA-Topo I covalent complex and inducing DNA double-strand breaks. XSJ151-induces DNA damage activates the p53-p21 signaling pathway, specifically regulating the expression of cyclins, leading to G2/M phase cell cycle arrest and disrupting the dynamic homeostasis of Bcl-2 family proteins, thereby triggering apoptosis in gastric cancer cells. XSJ151 can be used for the study of gastric cancer.

RR-171 is an amino acid polypeptide and an inhibitor of the Wnt signaling pathway. RR-171 reduces the expression levels of Wnt-1, GSK3β and β-catenin. RR-171 induces apoptosis (Apoptosis) in pancreatic cancer cells, which is characterized by an increased Bax/Bcl-2 ratio, activation of Caspase-3/7/9, and increased Cleaved-PARP; this pro-apoptotic effect can be partially reversed by Z-VAD-FMK (HY-16658B). RR-171 also induces pyroptosis (Pyroptosis) in pancreatic cancer cells, which is manifested by activation of the NLRP-3 inflammasome, activation of Caspase-1, cleavage of GSDMD, upregulation of IL-1β and IL-18, and increased LDH release; this pro-pyroptotic effect can be partially reversed by VX-765 (HY-13205). RR-171 inhibits the viability, proliferation and colony formation of pancreatic cancer cells, with low cytotoxicity against normal cells. RR-171 downregulates the expression of Ki-67 and PCNA in tumor tissues in vivo, with favorable biosafety. RR-171 can be used in studies related to pancreatic cancer.

Anticancer agent 65 (compound 4c) shows excellent activity in cancer cell lines, especially A549 cells, with an IC₅₀ of 1.07 μM. Anticancer agent 65 induces S-phase arrest in A549 cells and increases the expression level of p53 and p21. Anticancer agent 65 causes apoptosis, ROS generation and collapse of MMP in A549 cells.

Glycocholic acid (sodium) (Standard) is the analytical standard of Glycocholic acid sodium (HY-N1423A). This product is intended for research and analytical applications. Glycocholic acid sodium is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid sodium inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid sodium modulates related bile acid receptor signaling. Glycocholic acid sodium suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid sodium can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).

EGFR-IN-191 is an anti-tumor agent targeting both EGFR and AKT. EGFR-IN-191 exerts its anti-tumor activity by inducing DNA damage, apoptosis, cell cycle arrest, and inhibition of the PI3K/AKT-EGFR signaling pathway in tumor cells. EGFR-IN-191 can be used in the study of tumors such as triple-negative breast cancer.

Anticancer agent 63 (compound 3h) shows active in reducing the viability of different cancer cell lines, including SW480, HeLa, A549 and MCF-7, with IC₅₀ values at 24 h of 4.9, 11.5, 9.4, and 3.4 μM, respectively. Anticancer agent 63 induce apoptosis in MCF-7 cells via down-regulating the expression of Bcl-2 and up-regulating the expression of IL-2 and Caspase-3. Anticancer agent 63 also shows antioxidant activity.

Apoptosis inducer 56 is an apoptosis inducer. Apoptosis inducer 56 induces DNA damage (upregulation of γH2AX and p-ATM expression) by minor groove binding. Apoptosis inducer 56 induces intrinsic apoptosis (upregulation of p53 and Bax/Bcl-2 ratio, cleaved caspase-7) via S-phase cell cycle arrest. Apoptosis inducer 56 shows selectivity for cancer cells over normal breast epithelial cells. Apoptosis inducer 56 can be used for the research of breast cancer.

Dihydrocapsaicin-d₃ is the deuterium labeled Dihydrocapsaicin (HY-N0361). Dihydrocapsaicin, a capsaicin, is a potent and selective TRPV1 (transient receptor potential vanilloid channel 1) agonist. Dihydrocapsaicin reduces AIF, Bax, and Caspase-3 expressions, and increased Bcl-2, Bcl-xL and p-Akt levels. Dihydrocapsaicin enhances the hypothermia-induced neuroprotection following ischemic stroke via PI3K/Akt regulation in rat.

FLC-8 is an orally active FLT3 inhibitor with IC₅₀ values of 10.2 nM, 11.6 nM and 24.10 nM against human FLT3-WT, FLT3-G697R and FLT3-N676D, respectively. FLC-8 inhibits FLT3 autophosphorylation and downstream STAT5, AKT and ERK signaling pathways, and induces apoptosis in acute myeloid leukemia (AML) cells. FLC-8 exhibits potent antitumor activity in the MV4-11 xenograft model. FLC-8 can be used for the research of acute myeloid leukemia.

Proquinazid is a Bcl-2 and PCNA modulator, oxidative stress inducer, genotoxin and apoptosis inducer. Proquinazid causes DNA damage and also triggers apoptosis by regulating pro-apoptotic and anti-apoptotic proteins.

PARP1-IN-58 is a ROS-responsive prodrug constructed based on a natural stilbene scaffold, and its active parent nucleus 24c acts as a selective PARP-1 inhibitor. PARP1-IN-58 only hydrolyzes to release the active parent compound in the high-ROS microenvironment of tumors; the active parent compound competitively binds to PARP-1 and blocks DNA single-strand damage repair, upregulates intracellular ROS levels, reduces mitochondrial membrane potential, and thereby induces cell cycle arrest and mitochondria-dependent apoptosis. PARP1-IN-58 exerts potent proliferation-inhibiting effects on BRCA-deficient breast cancer cells under simulated tumor oxidative stress conditions, and exhibits tumor growth inhibitory activity in breast cancer xenograft models. PARP1-IN-58 can be used in cancer-related research.

NEURL1B-IN-1 is a molecular glue-like NEURL1B degrader with a Kd value of 46.2 nM. NEURL1B-IN-1 binds to Arg422 within the NHR2 domain of NEURL1B, triggers its autoubiquitination and proteasomal degradation, disrupts its interaction with DLL1, and attenuates the Notch signaling pathway. NEURL1B-IN-1 induces cell cycle arrest and apoptosis, and inhibits migration of hepatocellular carcinoma cells. NEURL1B-IN-1 is applicable to research related to hepatocellular carcinoma.

Clausenidin is a selective inhibitor targeting apoptosis-related pathways, including the mitochondrial pathway and death receptor pathway, and vascular endothelial growth factor (VEGF). Clausenidin induces mitochondrial membrane depolarization by activating caspase-3, caspase-8 and caspase-9, upregulating the pro-apoptotic protein Bax and downregulating the anti-apoptotic protein Bcl-2. Clausenidin also inhibits VEGF expression and blocks angiogenesis, exerting anti-tumor activity. Clausenidin has inhibitory effects against Mycobacterium tuberculosis (MIC=200 μg/mL). Clausenidin can induce apoptosis in liver cancer cells, arrest the cell cycle in the G2/M phase, and inhibit tumor angiogenesis. Clausenidin can be used in the research of malignant tumors such as liver cancer.

Hsp90-IN-42 is a heat shock protein 90 (Hsp90) inhibitor with an IC₅₀ of 15.65 nM against human targets. Hsp90-IN-42 destabilizes EGFR and inhibits the activation of the EGFR-Akt signaling pathway. Hsp90-IN-42 suppresses the proliferation and migration of cancer cells, induces cell cycle arrest by downregulating CDK12 and CDK13, and triggers mild apoptosis via downregulating Bcl-2 and upregulating Bax. Hsp90-IN-42 inhibits tumor growth in xenograft mouse models. Hsp90-IN-42 can be used in research related to colorectal cancer.

MI-223 is a Mcl-1 regulator (K_d = 160 nM). MI-223 binds to the BH1 domain, blocking Mcl-1-stimulated homologous recombination DNA repair, thus sensitizing cancer cells to DNA replication agents. MI-223 can be used in research on cancers such as lung cancer.

MAHS-4 is an inhibitor of thymidylate synthase (TS) and dihydrofolate reductase (DHFR), with IC₅₀ values of 1.918 μM and 83.53 μM, respectively. MAHS-4 inhibits thymidylate biosynthesis, reduces tetrahydrofolate pool maintenance, and interferes with extracellular matrix remodeling. MAHS-4 induces G2/M phase cell cycle arrest, activates endogenous caspase-dependent apoptosis, decreases MMP protein levels, inhibits cell migration, increases intracellular NO levels, and promotes autophagy activity. MAHS-4 is applicable for cancer-related research.

Amantadine in Methanol (Standard) is the solution of Amantadine (Standard). This product is intended for research and analytical applications. Amantadine (1-Adamantanamine) is an orally avtive and potent antiviral agent with activity against influenza A viruses. Amantadine inhibits several ion channels such as NMDA and M2, and also inhibits Coronavirus ion channels. Amantadine also has anti-orthopoxvirus and anticancer activity. Amantadine can be used for Parkinson's disease, postoperative cognitive dysfunction (POCD) and COVID-19 research[4].

Barakol is an anticancer and anxiolytic agent identified in Cassia siamea. Barakol inhibits MMP-3 activity and enhances the cytotoxicity and antimetastatic effects of Doxorubicin (HY-15142) against cancer cells. Barakol induces apoptosis via reactive oxygen species (ROS) production, upregulation of the Bax/Bcl-2 protein ratio, and activation of caspase-9. Barakol exerts anxiolytic activity with diazepam-like effects, increases spontaneous longitudinal smooth muscle contraction of rat ileum in a concentration-dependent manner (EC₅₀ = 0.3 mM), and inhibits norepinephrine-induced contraction suppression. Barakol can be used in research related to anxiety, intestinal motility, and neuroblastoma.

Fucoxanthinol, a carotenoid, is a deacetylated Fucoxanthin (HY-N2302) metabolite with oral activity, and inhibits rat pancreatic lipase with an IC₅₀ of 764 nM. Fucoxanthinol reduces expression of Bcl-2, Bcl-xL, survivin, XIAP, cIAP2, cyclin D1, cyclin D2, cyclin E, CDK4, CDK6, β-catenin, JunD, PPARγ, and induces GADD45α expression. Fucoxanthinol activates caspase-3, caspase-8, caspase-9, Nrf2/Keap1/ARE pathway, and inhibits activation of Akt, NF-κB, AP-1, PDPK1, GSK3β phosphorylation. Fucoxanthinol induces apoptosis, G0/G1 cell cycle arrest, inhibits cancer cell viability, proliferation, migration, invasiveness, tumour growth, adipocyte differentiation, oxidative stress, neurotoxicity, triglyceride absorption, angiogenesis, and obesity-induced inflammation. Fucoxanthinol can be used for the research of osteosarcoma, leukemia, lymphoma, adult T-cell leukemia, prostate cancer, colon cancer, breast cancer, hypertriglyceridaemia, Alzheimer’s disease, Parkinson’s disease, obesity, insulin resistance, malignant melanoma, and type II diabetes.