bcl-2-in-1

MCL-1 BCL-2-IN-2 (Compound Nap-1) is a potent and selective dual inhibitor of Mcl-1 and Bcl-2, with IC50 values of 4.45 μM and 3.18 μM, respectively [1].

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

MCL-1 BCL-2-IN-3 is a selective and potent dual inhibitor of Mcl-1 and Bcl-2, with IC50 values of 5.95 and 4.78 μM, respectively.

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

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

Bcl-2 Mcl-1-IN-2 is an inhibitor of Bcl-2 [Ki: 4.70 μM] and Mcl-1 [Ki: 0.88 μM], suitable for use in cancer research.

Bcl-2 Mcl-1-IN-3 is a Bcl-2 Mcl-1 inhibitor, targeting Mcl-1 (Ki: 0.14 μM) and Bcl-2 (Ki: 0.23 μM), suitable for cancer research.

Bcl-2-IN-11 (compound 6) is a potent and selective Bcl-2 activity inhibitor with an IC50 of 0.9 nM and minimal inhibition against Bcl-xl (IC50 > 1000 nM). It is used in cancer research related to Bcl-2 family protein overexpression, particularly in hematologic malignancies like acute lymphoid leukemia, while minimizing the risk of side effects such as thrombocytopenia [1] by sparing Bcl-xl.

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

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

Bcl-2-IN-14 (Compound 13c), a BCL-2 inhibitor with an inhibitory concentration (IC50) of 0.471 μM, is applicable in cancer research [1].

Bcl-2-IN-13, a potent Bcl-2 inhibitor with an IC50 of 17 nM, shows promise for cancer research applications [1].

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

Bcl-2-IN-17, a Bcl2 inhibitor, is utilized for researching diseases associated with the Bcl anti-apoptotic protein [1].

Bcl-2 Mcl-1-IN-4 (compound 20) acts as a dual inhibitor targeting Bcl-2 (Ki=0.49 μM) and Mcl-1 (Ki=0.51 μM). This compound effectively suppresses cancer cell proliferation and induces apoptosis in U937 cells. It is utilized in cancer research.

1. Dehydrocorydaline (13-Methylpalmatine) exerts anti-metastatic potential via suppression of MMPs and Bcl-2 signaling in NSC-LC cells. 2. Dehydrocorydaline stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. 3. Dehydrocorydaline shows antiplatelet effects, it inhibits thrombin-induced platelet aggregation in a low dose ( IC50= 34.914 ug mL). 4. Dehydrocorydaline has anti-inflammatory and antinociceptive effects. 5. Dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax Bcl-2, activating caspases as well as cleaving PARP.

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.

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.

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.

A-1211212 (BCL2-IN-1) is a potent and selective Bcl-2 inhibitor. It promotes lymphocyte apoptosis, alters colonic mucosa in mice, and improves inflammation.

Nitroaspirin (NCX 4016) is a nitric oxide donor and a nitro-derivative of Aspirin that inhibits cyclooxygenase. It induces cell cycle arrest and apoptosis in Cisplatin-resistant human ovarian cancer cells by down-regulating EGFR PI3K STAT3 signaling and modulating Bcl-2 family proteins. Additionally, Nitroaspirin possesses antithrombotic and antiplatelet properties and acts as a direct and irreversible inhibitor of COX-1.

Mcl1-IN-11 (Compound G) is a selective Mcl-1 inhibitor with Kis of 0.06 μM and 4.2 μM for Mcl-1 and Bcl-2, respectively.

Mcl1-IN-12 has anti-tumor activity.It is a selective Mcl-1 inhibitor, less potent at Bcl-2, with Kis of 0.29 and 3.1 μM, respectively.

VDR agonist 1 (compound 28), a nonsteroidal Vitamin D receptor (VDR) agonist, demonstrates potent activity with a low IC 50 of 690 nM in MCF-7 cells. It inhibits cell cycle progression through upregulation of p21 and p27, and induces apoptosis by elevating BAX expression while reducing Bcl-2 levels [1].