Bax Modulator

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.

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.

Ferroptosis/apoptosis inducer-5 is an orally active inducer of Ferroptosis and Apoptosis. Ferroptosis/apoptosis inducer-5 downregulates GPX4, upregulates ACSL4, promotes ROS production, activates the Caspase cascade, induces Mitochondrial dysfunction, and alters the Bcl-2/Bax balance. Ferroptosis/apoptosis inducer-5 significantly inhibits tumor growth in a pancreatic cancer xenograft mouse model. Ferroptosis/apoptosis inducer-5 can be used for the research of pancreatic cancer.

EGFR/CDK2-IN-5 is a potent dual EGFR and CDK2 inhibitor with IC₅₀s of 17.30 and 212.10 nM, respectively. EGFR/CDK2-IN-5 also inhibits EGFR^T790M with an IC₅₀ of 123.8 nM. EGFR/CDK2-IN-5 exhibits potent anticancer activity. EGFR/CDK2-IN-5 induces G1 and S cell cycle arrest and apoptosis, accompanied by increased levels of caspase-3/9 and Bax, as well as decreased Bcl-2 levels. EGFR/CDK2-IN-5 can be used for the research of cancers, such as lung cancer, breast cancer, and leukemia.

PI3K-IN-58 (Compound 17f) is a PI3Kα inhibitor (IC₅₀: 0.039 μM). PI3K-IN-58 exhibits significant antiproliferative effects on PC-3, 22RV1, MDA-MB-231 and MDA-MB-453 cell lines with IC_50s of 3.48 μM, 1.06 μM, 2.21 μM and 0.93 μM, respectively. PI3K-IN-58 induces apoptosis by downregulating the expression levels of anti-apoptotic proteins Bcl-XL and Bcl-2 and upregulating the expression of anti-apoptosis protein BAX. PI3K-IN-58 can be used in PI3K-targeted cancer research.

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.

α-D-Manp(3→1)-α-D-Manp(2→1)-α-D-Glu (Compound C) is an oligosaccharide. α-D-Manp(3→1)-α-D-Manp(2→1)-α-D-Glu activates the PI3K/AKT signaling pathway. α-D-Manp(3→1)-α-D-Manp(2→1)-α-D-Glu significantly inhibits Apoptosis by regulating the Bcl-2/BAX ratio. α-D-Manp(3→1)-α-D-Manp(2→1)-α-D-Glu shows cytoprotective activity by reducing ROS and LDH levels, decreasing MDA activity, and increasing CAT, SOD, and GSH activities. α-D-Manp(3→1)-α-D-Manp(2→1)-α-D-Glu shows neuroprotective effects and antioxidant capacity.

Anticancer agent 64 (compound 5m) shows cytotoxic activity in CCRF-CEM cells, with IC₅₀ of 2.4 μM. Anticancer agent 64 shows good anticancer activity through apoptosis induction. Anticancer agent 64 induces caspase 3 and 7 activation and PARP cleavage. Anticancer agent 64 induces significant effect of mitochondria depolarization.

Bcl-2-IN-6 (compound 10) is a potent Bcl-2 (B-cell lymphoma-2) inhibitor. Bcl-2-IN-7 down-regulates the expression of Bcl-2, and increases the expression of p53, Bax, and caspase-7 mRNA. Bcl-2-IN-7 induces cell cycle arrest and apoptosis in breast cancer MCF-7 cells. Bcl-2-IN-7 shows good anticancer activity, with IC₅₀ values of 20.91, 22.30, 42.29, and 48.00 μM against MCF-7, LoVo, HepG2, and A549 cell lines, respectively.

Bcl-2-IN-7 (compound 6) is a potent Bcl-2 (B-cell lymphoma-2) inhibitor. Bcl-2-IN-7 down-regulates the expression of Bcl-2, and increases the expression of p53, Bax, and caspase-7 mRNA. Bcl-2-IN-7 induces cell cycle arrest and apoptosis in breast cancer MCF-7 cells. Bcl-2-IN-7 shows good anticancer activity, with IC₅₀ values of 20.17, 22.64, 45.57, and 51.50 μM against MCF-7, LoVo, HepG2, and A549 cell lines, respectively.

Astin B is a orally active and potent cyclic pentapeptide, that can be isolated from Aster tataricus. Astin B has hepatotoxic effects in vitro and in vivo and that hepatic injury was primarily mediated by apoptosis in a mitochondria/caspase-dependent manner. Astin B induces autophagy in L-02 cells, increases LC3-II and decreases p62 expression.

COX/5-LO-IN-2 is a COX2, EGFR, COX1, 5-LOX, BRAF and FAK inhibitor with IC₅₀ of 1.22 μM, 2.5 μM, 2.95 μM, 4.65 μM, 7.4 μM, 12.2 μM, respectively. COX/5-LO-IN-2 induces cell growth arrest at G2/M phase. COX/5-LO-IN-2 triggers apoptotic activity by up-regulating proapoptotic proteins p53, Bax, and caspase-7 and down-regulating anti-apoptotic protein Bcl-2. COX/5-LO-IN-2 can be used for the research of breast cancer.

Dehydrobruceine B, a quassinoid, can be isolated from Brucea javanica. Dehydrobruceine B shows a synergistic effect with Cisplatin (HY-17394) to induce apoptosis via mitochondrial method. Dehydrobruceine B increases apoptosis-inducing factor (AIF) and Bax expression and suppresses Keap1-Nrf2.

Aurora kinase-IN-15 is a potent dual Aurora A and Aurora B kinase inhibitor. Aurora kinase-IN-15 has broad-spectrum anticancer activity and low toxicity to normal cells. Aurora kinase-IN-15 induces G₂/M phase arrest, apoptosis, and activates the intrinsic apoptotic pathway through upregulation of Caspase 3 and Bax, along with downregulation of Bcl-2. Aurora kinase-IN-15 can be used for the study of breast cancer, hepatocellular carcinoma, colorectal cancer and prostate cancer.

CDC25A/NF-κB-IN-1 is an effective dual-target inhibitor of CDC25A and NF-κB, and is a prodrug of Pt(IV). CDC25A/NF-κB-IN-1 has anticancer activity and low cytotoxicity to normal cells. CDC25A/NF-κB-IN-1 can trigger a variety of anticancer mechanisms, including S phase cell cycle arrest, mitochondrial endogenous apoptosis, endoplasmic reticulum stress, autophagy-dependent ferroptosis. CDC25A/NF-κB-IN-1 has good safety and can be used for ovarian cancer research.

Topoisomerase I-IN-23 is a topoisomerase I inhibitor with anticancer activity. Topoisomerase I-IN-23 competitively binds to the hydrophobic pocket at the Topo I-DNA interface, stabilizes the covalent DNA-Topo I complex, downregulates Topo I protein expression in a concentration-dependent manner, induces S-phase cell cycle arrest in tumor cells, regulates the expression of apoptosis-related proteins Bax, Bcl-2 and cleaved caspase-3 to trigger apoptosis, and inhibits the migration and invasion of tumor cells. Topoisomerase I-IN-23 exhibits in vivo antitumor efficacy in xenograft models. Topoisomerase I-IN-23 can be used in research related to colorectal cancer, lung cancer and hepatocellular carcinoma.

Desethylamiodarone hydrochloride (Standard) (N-Desethylamiodarone hydrochloride (Standard); LB 33020 hydrochloride (Standard)) is the analytical standard of Desethylamiodarone hydrochloride (HY-130353). This product is intended for research and analytical applications. 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.

Anticancer agent 306 is a spiro tetramic acid derivative and a inhibitor of MMP1, MMP7 and PLK1. Anticancer agent 306 exerts antiproliferative activity against H1299, RKO and MCF-7 cells with IC₅₀ values of 19.25 μM, 3.29 μM and 102.36 μM, respectively. Anticancer agent 306 can up-regulate p21 protein and down-regulate CCND1 and CCNB1 proteins to induce cell cycle arrest, regulate the expression of Bcl-2 and Bax to induce cell apoptosis. Anticancer agent 306 can down-regulate MMP1 and MMP7 proteins to inhibit tumor invasion and metastasis. Anticancer agent 306 can be used for the research of lung cancer, colorectal cancer, breast cancer.

Swerchirin is an orally active, plant-derived xanthone that acts as an inhibitor of the Raf/MEK/ERK signaling pathway. Swerchirin downregulates the expression of phosphorylated MEK and phosphorylated ERK, induces mitochondrial apoptosis and cell cycle arrest, regulates Bcl-2 family proteins, triggers cytochrome c release, activates caspases, and drives PARP cleavage. Swerchirin reduces blood glucose levels in rat models under fasting, fed, glucose-loaded conditions, and following treatment with Tolbutamide (HY-B0401). Swerchirin can be used in research related to ovarian cancer, liver injury, and diabetes.

ERK5-IN-7 is an orally active ERK5 inhibitor with an IC₅₀ of 403.4 nM. ERK5-IN-7 directly inhibits ERK5 kinase activity, and downregulates the phosphorylation level and total protein expression of ERK5. ERK5-IN-7 induces Apoptosis (upregulates Bax, downregulates Bcl-2, and induces Caspase-3 cleavage). ERK5-IN-7 induces ROS accumulation. ERK5-IN-7 exhibits anticancer effects against Lewis lung cancer.