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Cat No. Product Name Synonyms Targets
T38622 Bcl-xL antagonist 2 BCL
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 l...
T77571 Bcl-B inhibitor 1 Apoptosis , BCL
Bcl-B inhibitor 1 is a Bcl-B inhibitor with antitumor activity that binds to and inactivates pro-apoptotic proteins in the BH3 structural domain.
T10483 Lisaftoclax Bcl-2/Bcl-xl inhibitor 1,APG-2575 BCL
Lisaftoclax (Bcl-2/Bcl-xl inhibitor 1) is an oral dual inhibitor of Bcl-2 and Bcl-xl, with IC50 values of 2 nM and 5.9 nM for Bcl-2 and Bcl-xl, respectively. Lisaftoclax is used to treat chronic lymphocytic leukemia (CLL...
T39961 Bcl-2-IN-2 Others
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 exhi...
T11969 MCL-1/BCL-2-IN-2 Others
MCL-1/BCL-2-IN-2 is a potent and selective Bcl-2 and Mcl-1 dual inhibitor.
T11970 MCL-1/BCL-2-IN-3 Others
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.
T11971 MCL-1/BCL-2-IN-4 Others
MCL-1/BCL-2-IN-4 is a selective and potent Mcl-1 and Bcl-2 dual inhibitor.
T11968 MCL-1/BCL-2-IN-1 BCL
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].
T79171 Bcl-2-IN-11 Others
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 ...
T74297 Bcl-2-IN-4 Others
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 effectiv...
T82912 Bcl-2-IN-14 Others
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].
T63676 Bcl-2-IN-6 Others
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...
T82910 Bcl-2-IN-16 Others
Bcl-2-IN-16 is a Bcl-2 (B-cell lymphoma 2) inhibitor [1].
T64053 Bcl-2-IN-8 Others
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 b...
T80221 TAT-BH4 (Bcl-xL) Apoptosis
TAT-BH4 (Bcl-xL), primarily localized at the mitochondria, inhibits apoptotic cell death. This compound comprises an N-terminal eosin-labeled cysteine and the protein transduction domain of the HIV TAT protein (amino aci...
T74138 PROTAC Bcl-xL degrader-2 PROTACs
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.
T73999 PROTAC Bcl-xL degrader-3 Others
PROTAC Bcl-xL degrader-3 is a potent ROTAC Bcl-xL degrader.
T80222 TAT-BH4 (Bcl-xL) (TFA) Apoptosis
"TAT-BH4 (Bcl-xL) TFA, primarily localized at the mitochondria, inhibits apoptotic cell death. This compound comprises an eosin-labeled cysteine at the N-terminal and the protein transduction domain from the HIV TAT prot...
T74298 Bcl-2-IN-5 Others
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...
T63757 Bcl-2-IN-9 Others
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.
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