bcl-b

Rasagiline (AGN1135) is an inhibitor of monamine oxidase used as adjunctive therapy in combination with levodopa and carbidopa in the management of Parkinsons disease.

Obatoclax (GX15-070), a pan-BCL-2 family proteins inhibitor and BH3 mimetic, exhibits a binding affinity (K_i) of 220 nM for BCL-2. It promotes autophagy-dependent cell death and cyclin D1 degradation via the proteasome. Additionally, Obatoclax demonstrates anti-cancer properties and broad-spectrum antiparasitic activity.

Gambogic Acid (Guttic Acid) ( EC50=0.78-1.64 uM) activates caspases. Gambogic Acid competitively suppresses Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1. The IC50s of Gambogic Acid for Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 are 1.47, 1.21, 2.02, 0.66, 1.06 and 0.79 uM, respectively.

1. Flavokawain B (Flavokavain B) has potent anti-inflammatory activity, can significantly inhibit production of NO and PGE2 in LPS-induced RAW 264.7 cells. 2. Flavokawain B, the hepatotoxic constituent from kava root, induces GSH-sensitive oxidative stress through modulation of IKK NF-κB and MAPK signaling pathways. 3. Flavokawain B induces apoptosis, has the potential usefulness of FKB for prevention and treatment of hormone-refractory prostate cancer in an adjuvant setting. 4. Flavokawain B acts through ROS generation and GADD153 up-regulation to regulate the expression of Bcl-2 family members, thereby inducing mitochondrial dysfunction and apoptosis in HCT116 cells.

CAY10404 (3-(4-METHYLSULPHONYLPHENYL)-4-PHENYL-5-T) is a potent and highly selective inhibitor of COX-2 and COX-1. It is also a potent inhibitor of PKB Akt and MAPK signalling pathways and induces apoptosis in NSC-LC cells, with analgesic, anti-inflammatory and anti-cancer activities.

BCL6-IN-6 is an inhibitor of Bcl-6 and can be used in studies about diffuse large B-cell lymphoma. BCL6-IN-6 blocks the interaction of Bcl-6 with its corepressors and dose-dependently reactivates Bcl-6 target genes.

Ridaifen-B, a tamoxifen derivative, works by inducing independent autophagy of Bcl-2, without estrogen receptor involvement.

Antimycin A4 is an active component of the antimycin A antibiotic complex that is more polar than antimycin A1 , antimycin A2 , and antimycin A3 . Antimycin A4 inhibits ATP-citrate lyase with a Ki value of 64.8 μM. The antimycin A complex is a mixture of antimycins A1, A2, A3, and A4 that demonstrates antifungal, insecticidal, nematocidal, and piscicidal properties. It blocks mitochondrial respiration and can deplete cellular levels of ATP via inhibition of complex III of the mitochondrial electron transport chain (ETC). Antimycin A prevents the transfer of electrons between the b-cytochromes and ubiquinone at the Q(inner) site of complex III. This results in the stabilization of the ubisemiquinone radical at the Q(outer) site of complex III, leading to increased production of superoxide. Antimycin A is widely used in research to shunt electron flow through the ETC to study the chemical details of oxygen respiration. Additionally, antimycin A has been shown to inhibit Bcl-2 and Bcl-xL proteins, inducing apoptosis.

Bcl-2-IN-16 is an inhibitor of Bcl-2 (B-cell lymphoma 2) [1].

1. Schisandrol B (Besigomsin) may exert neuroprotective effects by attenuating the microglia-mediated neuroinflammatory response via inhibiting the TLR4-mediated NF-κB and MAPKs signaling pathways. 2. Schisandrol B has anti-inflammatory property, potentially result from the inhibition of COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation. 3. Schisandrol B induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway. 4. Schisandrol B significantly inhibits cell proliferation in a dose-dependent manner, due to cell cycle arrest in the G1 phase with the downregulation of cyclin D1 expression and Retinoblastoma (RB) phosphorylation.

1. β,β-Dimethylacrylshikonin (Dimethylacrylshikonin) is a promising agent for developing an improved strategy for radiotherapy against tumors. (a) Injection of Dimethylacrylshikonin combined with IR treatment significantly suppressed tumor growth of the HCT-116 xenograft. (b) Dimethylacrylshikonin significantly suppressed the growth of H(22) transplantable hepatoma, and induced the activation of caspase-3 . (c) Dimethylacrylshikonin inhibited growth of gastric cancer SGC-791 cells by inducing ERK signaling pathway. 2. Dimethylacrylshikonin inhibits the proliferation of MCF-7 cells in vitro by inducing apoptosis through the downregulation of Bcl-2, upregulation of Bax and partial inactivation of the NF-κB pathway.

Lucidenic acid B (Lucidenicacid B), a natural compound extracted from Ganoderma lucidum, induces activation of caspase-9 and caspase-3 and cleavage of PARP, which can induce apoptosis in human leukemia cells through mitochondrial mediation. Lucidenic acid B inhibits PMA-induced invasion of human hepatocellular carcinoma cells by inactivating the MAPK ERK signaling pathway and decreasing the binding activity of NF-kappaB and AP-1. Lucidenic acid B had no effect on cell cycle and necrotic cells.

Lonitoclax is an inhibitor of B-cell lymphoma 2 (Bcl-2). It demonstrates antitumor activity in B-cell and myeloid malignancy models comparable to Venetoclax. Lonitoclax holds potential for research in relapsed or refractory chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma, and certain low-grade lymphomas.

Destruxin B is a cyclic peptide with insecticidal and anticancer activity isolated from the insect pathogenic fungus Metarhizium isopliae. Destruxin B induces apoptosis of human non-small cell lung cancer cells through the Bcl-2 family-dependent mitochond

MLS-0053105, a chloromaleimide, functions as a selective inhibitor of BFL-1, exhibiting an IC50 of 0.4 µM against Bfl-1 F-Bid. Its inhibitory potency is over tenfold lower for Bcl-W, Bcl-2, and Bcl-XL, and it shows no activity against Bcl-B and Mcl-1.

BCL6-IN-8c is an orally active and potent inhibitor of B-cell lymphoma 6 (BCL6)-corepressor interaction(IC50 of 0.10 μM in cell-free enzyme-linked immunosorbent assay).

Safflor Yellow B mitigates angiotensin II-induced injury in human umbilical vein cells by modulating Bcl-2 p22(phox) expression and demonstrates neuroprotective effects [1].

Bcl-2-IN-6 is a potent inhibitor of Bcl-2 (b-cell lymphoma-2) that downregulates Bcl-2 expression 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 acts on MCF-7 cells ( Bcl2-IN-7 showed good antitumor effects on MCF-7 cells (IC50: 20.91 μM), LoVo cells (IC50: 22.30 μM), HepG2 cells (IC50: 42.29 μM) and A549 cells (IC50: 48.00 μM).

DHA-paclitaxel, also know as Taxoprexin, is prodrug comprised of the naturally occurring omega-3 fatty acid docosahexaenoic acid (DHA) covalently conjugated to the anti-microtubule agent paclitaxel. Because tumor cells take up DHA, DHA-paclitaxel is delivered directly to tumor tissue, where the paclitaxel moiety binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. Paclitaxel also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2). DHA-paclitaxel exhibits improved pharmacokinetic and toxicity profiles when compared to conventional paclitaxel and has demonstrated antineoplastic activity in animal models of cancer.