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

Bcl-2-IN-14 (Compound 13c), a BCL-2 inhibitor, exhibits an inhibitory concentration (IC 50) of 0.471 μM, and is applicable in cancer research [1].

Bcl-2-IN-12 (Compound 1) is a potent Bcl-2 inhibitor with an IC50 value of 6 nM, utilized in cancer research [1].

Bcl-2-IN-15 (Compound 13d) is a Bcl-2 inhibitor with an IC50 of 363 nM, which impedes the proliferation of the NCI leukemia cancer cell line [1].

Bcl-2-IN-5 is a potent inhibitor of BCL-2, demonstrating inhibitory concentrations (IC50) of 0.12 nM, 0.14 nM, and 0.22 nM against wild type Bcl-2, Bcl-2 D103Y, and Bcl-2 G101V, respectively. Additionally, it effectively suppresses cell growth in Bcl 2-G101V knock-in RS4;11 cells, with IC50 values of 0.2 nM and 0.44 nM.

Bcl-xL antagonist 2 is an effective and selective antagonist of Bcl-xL with an IC50 of 91 nM and a Ki of 65 nM. Bcl-xL antagonist 2 induces apoptosis in cancer cells and can be used in studies about chronic lymphocytic leukemia and non-Hodgkin’s lymphoma.

Bcl-2-IN-13 is a potent inhibitor of Bcl-2, exhibiting an IC50 of 17 nM, and holds potential for use in cancer research [1].

Beclin1-Bcl-2 Interaction Inhibitor 1 effectively disrupts the binding of Beclin 1 to Bcl-2, and is utilized in cancer and neurodegeneration research [1].

MCL-1/BCL-2-IN-4 is a selective and potent Mcl-1 and Bcl-2 dual inhibitor.

Bcl-2-IN-9 is a novel, pro-apoptotic, low cytotoxic Bcl-2 inhibitor (IC50: 2.9 μM). Bcl-2-IN-9 downregulates Bcl-2 expression, induces apoptosis in cancer cells, and exhibits high selectivity for leukemia cells.

Bcl-2-IN-4, an orally active and selective inhibitor of Bcl-2, demonstrates potent efficacy with an IC50 value of 1.5 nM and exhibits more than 200-fold selectivity over Bcl-xL (IC50 of 411 nM). Additionally, it effectively inhibits the proliferation of RS4;11 cells, achieving an IC50 of 2.7 nM.

Bcl-2/Mcl-1-IN-3 is a Bcl-2/Mcl-1 inhibitor that acts on Mcl-1 (Ki: 0.14 μM) and Bcl-2 (Ki: 0.23 μM) and can be used in cancer research.

Bcl-2/Mcl-1-IN-2 is a Bcl-2 (Ki: 4.70 μM) and Mcl-1 (Ki: 0.88 μM) inhibitor.Bcl-2/Mcl-1-IN-2 can be used in cancer research.

CDK2/Bcl2-IN-1 (compound 1) is a saponin-based inhibitor of CDK-2 (IC50=117.6 nM) that exhibits potent cytotoxic effects on cancer cells. Additionally, it inhibits Bcl-2 and promotes apoptosis in A549 lung cancer cells [1].

Bcl-2-IN-7 is a potent inhibitor of Bcl-2 (b-cell lymphoma-2), which can downregulate the expression of Bcl-2, increase the expression of p53, Bax, caspase-7 mRNA, and induce cell cycle arrest and apoptosis in MCF-7 cells of breast cancer. Bcl2-IN-7 showed good antitumor activity against MCF-7 cells (IC50: 20.17 μM), LoVo cells (IC50: 22.64 μM), HepG2 cells (IC50: 45.57 μM) and A549 cells (IC50: 51.50 μM).

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).

MCL-1/BCL-2-IN-2 is a selective Mcl-1 and Bcl-2 inhibitor with potential antitumor activity for tumor research.

MCL-1/BCL-2-IN-3 is a selective and potent Mcl-1 and Bcl-2 dual inhibitor with IC50s of 5.95 and 4.78 μM, respectiely.

MCL-1/BCL-2-IN-2 (Compound Nap-1) is a potent and selective dual inhibitor of Mcl-1 and Bcl-2 with IC 50 s of 4.45 and 3.18 μM, respectively [1].

Bcl-2-IN-8 is a potent anti-cancer agent. bcl-2-IN-8 exhibits anti-proliferative effects on both drug-sensitive and drug-resistant cancer cells. bcl-2-IN-8 inhibits cell migration in a dose-dependent manner. bcl-2-IN-8 blocks the cell cycle in the G1 phase and induces apoptosis. bcl-2-IN-8 has shown research potential in triple-negative breast cancer. Bcl-2-IN-8 has shown potential for research in triple negative breast cancer.

Bcl-2-IN-11 (compound 6) is a potent and selective inhibitor of Bcl-2 activity, exhibiting an IC50 of 0.9 nM, and demonstrates minimal inhibition against Bcl-xl (IC50 > 1000 nM). This compound is utilized in researching various cancers linked to the overexpression of Bcl-2 family proteins, primarily malignant hematologic conditions such as acute lymphoid leukemia. Importantly, Bcl-2-IN-11 minimizes the risk of toxic side effects, including thrombocytopenia [1], by sparing Bcl-xl.

Bcl-2-IN-2 is a highly potent and selective inhibitor targeting Bcl-2 and Bcl-xL. It displays an IC50 value of 0.034 nM, suggesting its strong inhibitory activity specifically against Bcl-2. Additionally, Bcl-2-IN-2 exhibits an IC50 value of 43 nM against Bcl-xL, demonstrating over 1000-fold selectivity for Bcl-2 compared to Bcl-xL.

Bcl-2/Mcl-1-IN-1 is an inhibitor of Bcl-2 (Ki: 4.53 μM) and Mcl-1 (Ki: 1.19 μM).Bcl-2/Mcl-1-IN-1 can be used in cancer research.

PROTAC Bcl-xL degrader-2, based on von Hippel-Lindau ligand, is a potent degrader of Bcl-xL (a Bcl-2 family member), demonstrating an IC 50 of 0.6 nM.

Magnolin reduces the renal oxidative stress, suppresses caspase-3 activity, and increases Bcl-2 expression in vivo and in vitro. Magnolin has anti-inflammatory and antioxidative effects.

Vanillyl Alcohol (3-Methoxy-4-hydroxybenzyl alcohol) possesses anti-angiogenic, anticonvulsive, anti-inflammatory, anti-oxidant, neuroprotective, and anti-nociceptive activities. Vanillyl alcohol can effectively inhibit the cytotoxicity and improved cell viability in 1-methyl-4-phenylpyridinium (MPP+)-induced MN9D dopaminergic cells, it also can attenuate the elevation of reactive oxygen species (ROS) levels, decrease in the Bax/Bcl-2 ratio and poly (ADP-ribose) polymerase proteolysis.

TV 3279 is a novel ChE-MAI inhibitor , and the neuroprotective properties depend on their ability to induce the anti-apoptotic proteins PKC, Bcl-2, Bcl-x, and SOD, and to block the nuclear translocation of the pro-apoptotic enzyme glyceraldehyde phosphate dehydrogenase in PC-12 and neuroblastoma cells.

Nitroaspirin (NCX 4016) is a nitric oxide donor and a nitro-derivative of Aspirin, which combines with Nitroaspirin to inhibit cyclooxygenase. Nitroaspirin induces significant induction of cell cycle arrest and apoptosis in Cisplatin-resistant human ovarian cancer cells via down-regulation of EGFR/PI3K/STAT3 signaling and modulation of Bcl-2 family proteins. Nitroaspirin has antithrombotic and antiplatelet properties and acts as a direct and irreversible inhibitor of COX-1.

Ethyl gallate (gallic acid ethyl ester) obviously decreases cell proliferation in MDA-MB-231 and MCF-7 cells in a dose- and time-dependent manner, exhibits cytotoxicity in a dose-dependent manner. Ethyl gallate can inhibit the abilities of invasion of breast cancer in vitro by inhibiting the mRNA levels of MMP-9/MMP-2, phosphorylation of Akt and protein expression of NF-κB and inhibits hydrogen peroxide signaling, may represent an alternative class of vasopressors for use in septic shock. Also, Ethyl gallate suppresses proliferation and invasion in human breast cancer cells by modulating the PI3K/Akt pathway, which may contribute to inhibiting their downstream targets such as NF-κB p-65, Bcl-2/Bax, and mRNA levels of MMP-2 and MMP-9 in breast cancer cells, could be used as potential antioxidants with safe therapeutic application in cancer chemotherapy.

1. Linarin (Acacetin-7-O-rutinoside) (acacetin-7-O-β-d-rutinoside) shows selective dose dependent inhibitory effect on acetylcholinesterase. 2. Linarin alleviates GalN/LPS-induced liver injury by suppressing TNF-α-mediated apoptotic pathways. 3. Linarin prevents A beta-induced neurotoxicity through the activation of PI3K/Akt, which subsequently inhibits GSK-3b and up-regulates Bcl-2. 4. The piperine significantly enhanced the oral absorption of Linarin in rats by inhibiting P-glycoprotein mediated cellular efflux during the intestinal absorption and likely simultaneously by inhibiting the metabolism of Linarin.

Calycosin (Cyclosin) acts as a selective estrogen receptor modulator. Calycosin induces apoptosis in human ovarian cancer SKOV3 cells by activating caspases and Bcl-2 family proteins. Calycosin suppresses breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways. Calycosin has antineoplastic effects against osteosarcoma through inducing apoptosis showing in vitro and in vivo investigations. Calycosin was shown to induce angiogenesis in human umbilical vein endothelial cell cultures (HUVEC) in vitro. Calycosin may be an effective skin-lightening agent that regulates the expression of melanogenic enzymes. Calycosin exhibited tyrosinase inhibitory activity with an IC(50) value of 38.4 microM.

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.

Cimidahurinine can attenuate Doxorubicin (DOX)-induced cardiotoxicity in a dose-dependent manner with EC50 values of 45.79 uM; it protects against cardiotoxicity by decreasing reactive oxygen species (ROS) accumulation and downregulating apoptosis-related Bax/Bcl-2 proteins.

IMB-XH1 (Mcl1-IN-2) is a myeloid cell factor 1 (Mcl-1) inhibitor.

Co-treatment with Tanshinone IIB (TSB) significantly inhibits the DNA laddering, cytotoxicity and apoptosis of rat cortical neurons induced by staurosporine in a concentration-dependent manner; TSB also suppresses the elevated Bax protein and decreased bc

FB49 is a selective Bcl-2-associated athanogene 3 (BAG3) inhibitor with a Ki of 45 μM. It inhibits the proliferation of human tumoral cells without affecting the viability of human peripheral mononuclear cells. Additionally, FB49 arrests the cell cycle at the G1 phase and induces apoptosis and autophagy in treated medulloblastoma HD-MB03 cells [1].

CPM-1285 induces apoptosis by effectively inhibiting the function of intracellular Bcl-2 and associated death antagonists. It exhibits a high binding affinity for Bcl-2, with an IC50 of 130 nM, and has been demonstrated to decrease tumor burden in mice [1].

BM-1197, a highly potent and specific dual inhibitor of Bcl-2 and Bcl-xL, effectively targets these proteins with IC50 values of 3.5 nM and 5.2 nM for Bcl-2 and Bcl-xL, respectively. This compound demonstrates notable antitumor activity in both in vitro and in vivo settings.

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

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].

BCL2-IN-1 is a potent Bcl-2 inhibitor (Ki <0.01 nM).

9(E),11(E),13(E)-Octadecatrienoic acid (β-ESA) is a conjugated polyunsaturated fatty acid that is found in plant seed oils and in mixtures of conjugated linolenic acids synthesized by the alkaline isomerization of linolenic acid. It reduces growth of Caco-2 colon cancer cells in a dose-dependent and time-dependent manner. In vitro, β-ESA induces DNA fragmentation and upregulation of pro-apoptotic Bax mRNA. β-ESA decreases protein expression of the apoptosis suppression factor Bcl-2 and induces apoptosis in T24 bladder cancer cells via production of reactive oxygen species. It also inhibits bacterial fatty acid dioxygenase with a Ki value of 49 nM in vitro.

BAX-IN-1 is a potential selective inhibitor of Bcl-2-associated X protein (BAX).

Aranorosin is a fungal metabolite originally isolated from P. roseus. It has antimicrobial activity against B. subtilis, A. niger, and C. albicans when used at a concentration of 1 mg/ml. Aranorosin also reduces viability in apoptosis-resistant HeLa/Bcl-2 cells.

Astragaloside may protect against brain contusion and neuronal apoptosis after TBI by attenuating microglia activation in male rats. Astragalosides-induced apoptosis in NB4 cells may be associated with down-regulation of the expression of BCL-2 and NF-κB,

Scutebarbatine A shows significant antitumor effects on A549 cells in vivo and in vitro via mitochondria-mediated apoptosis by up-regulating expressions of caspase-3 and 9, and down-regulating Bcl-2. Scutebarbatine A and barbatine A show a significant ability to protect cells against H2O2 with ED50 values of 5.0 and 16.8 μM, respectively.

Crenulatin has dual- direction effects on apoptosis of cerebral microvascular endothelial cells, inhibitive effect in 25 mg/L and stimulative effect in 100 mg/L group, respectively; the mechanism is related to the alterations of Fas/Bcl-2 expression and caspase-3 activity.

XZ739 is a Cereblon-dependent PROTAC BCL-XL degrader, targeting a member of the Bcl-2 family, with a DC50 value of 2.5 nM in MOLT-4 cells after 16 hours of treatment. Additionally, XZ739 elicits cell death via caspase-mediated apoptosis.

Ginsenoside Rg6 can inhibit JK cell proliferation in human lymphocytoma and induce its apoptosis, the mechanism may through mitochondrial dysfunction and an increase of Bax expression and decrease of Bcl-2 expression.

Amygdalin (Laetrile) has antifibrotic, antitumor, anti-inflammatory and analgesic effects, amygdalin joint HSYA could inhibit the degeneration of the endplate chondrocytes derived from intervertebral discs of rats induced by IL-1beta and better than the single use of Amygdalin or HSYA. Amygdalin induces apoptotic cell death in human DU145 and LNCaP prostate cancer cells by caspase-3 activation through down-regulation of Bcl-2 and up-regulation of Bax.