mcl-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 inhibitor 3 shows good pharmacokinetic properties and excellent in vivo efficacy without toxicity.Mcl-1 inhibitor 3 is a highly potent and orally activate macrocyclic Mcl-1 inhibitor (Ki= 0.061 nM; IC50=19 nM in an OPM-2 cell viability assay).

MIK665 (S-64315) (S-64315) has an inhibitory effect on myeloid leukemia.

S63845 is a selective myeloid leukemia 1(MCL1) inhibitor that binds to human MCL1 with a Kd of 0.19 nM.

A09-003 is a novel cell cycle protein-dependent kinase-9 CDK-9 inhibitor.A09-003 inhibits the proliferation of a variety of leukemia cell lines and inhibits the increase of leukemia sequence-1 protein in myeloid cells.A09-003 also induces apoptosis, decreases RNA polymerase II activity, and decreases Mcl-1 expression.

BT2, a BCKDC kinase (BDK) inhibitor, exhibits an IC50 of 3.19 μM and functions as a potent, selective Mcl-1 inhibitor with a Ki value of 59 μM. Its interaction with BDK induces helix movements in the N-terminal domain, leading to BDK's dissociation from the branched-chain α-ketoacid dehydrogenase complex (BCKDC).

NH2-C6-NH-Boc is a PROTAC linker used in the synthesis of the Mcl-1 inhibitor [based on PROTAC].

Triacetylresveratrol (Acetyl-trans-resveratrol) has anti-cancer activity,it inhibits the phosphorylation of STAT3 and NFκB, down-regulates Mcl-1, and up-regulates Bim and Puma in pancreatic cancer cells.

Voruciclib is an orally active and selective CDK inhibitor (Ki: 0.626 nM-9.1 nM) that represses the expression of MCL-1 in multiple models of diffuse large B-cell lymphoma and effectively blocks CDK9, the transcriptional regulator of MCL-1.

AZD-5991, an antitumor compound, is a highly selective, potent and direct MCL-1 inhibitor that induces rapid apoptosis in cancer cells by activating the Bak-dependent mitochondrial apoptotic pathway, used for multiple myeloma, acute myeloid leukemia, and triple-negative inflammatory breast cancer.

PROTAC Bcl2 degrader-1 is a PROTAC, which potently and selectively induces the degradation of Mcl-1 (IC50: 11.81 μM) and Bcl-2 (IC50: 4.94 μM; DC50: 3.0 μM).

Maritoclax (Marinopyrrole A) (Marinopyrrole A) is a novel and specific Mcl-1 inhibitor, shows >8 fold selectivity than BCL-xl (IC50 > 80 μM),with an IC50 value of 10.1 μM.

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.

PROTAC Mcl1 degrader-1 is a Cereblon ligand-based targeted chimeric protein degrader (PROTAC), a selective Mcl-1 inhibitor. By hijacking the CRBN ubiquitin ligase to form a ternary complex with the target protein, it induces Mcl-1 ubiquitination. It can be used for cancer research.

Mcl1-IN-9 is a potent myeloid cell leukemia-1 (Mcl-1) inhibitor, exhibiting an IC50 of 446 nM in reengineered BCR-ABL+ B-ALL cells and a Ki of 0.03 nM.

MIM1 (Inhibitor of Mcl-1) is an myeloid cell factor 1 (Mcl-1) inhibitor.

(+)-Apogossypol is an antagonist of pan-BCL-2. (+)-Apogossypol binds to Mcl-1(Bcl-2 and Bcl-xL with EC50s of 2.6, 2.8 and 3.69 µM, respectively).

Tapotoclax (AMG-176) is an orally active MCL1 inhibitor for the study of myeloid leukemia.

Mcl1-IN-1 is a myeloid cell factor 1 inhibitor (IC50=2.4 µM).

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

CLZ-8 (Mcl1-IN-8) is an orally active inhibitor of Mcl-1-PUMA (p53 up-regulated mediator of apoptosis) with radioprotective properties.CLZ-8 ameliorates radiation-induced HUVEC cell damage and reduces apoptosis counts, and inhibits radiation-induced overexpression of PUMA.

MT 63-78 is a specific and effective direct AMPK activator (EC50: 25 μM) that blocks prostate cancer growth by inhibiting the lipogenesis and mTORC1 pathways. It has antitumor effects and induces cell mitotic arrest and apoptosis.