Bax 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.

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.

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.

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.

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.

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.

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.

Nivitol (UP302) is a natural phenolic compound discovered from Dianella ensifolia and also acts as a Tyrosinase inhibitor. Nivitol competitively and reversibly inhibits tyrosinase, suppressing melanin production. Nivitol inhibits homogentisate 1,2-dioxygenase (HGD). In human leukemia cells, Nivitol inhibits PI3K/AKT pathway phosphorylation, increases ROS, decreases mitochondrial membrane potential, and induces G2/M cell cycle arrest, apoptosis, and PINK1/Parkin-mediated mitophagy. Nivitol exhibits inhibition of tumor growth in the MV411 xenograft mouse model. Nivitol is used for research on exogenous ochronosis, hyperpigmentation, and leukemia.