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MitoBloCK-6

MCE China：MitoBloCK-6

Brand：MedChemExpress (MCE)

Cat. No.HY-122652

CAS：303215-67-0

Purity：98.07%

Storage：4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：MitoBloCK-6 is a potent Erv1/ALR inhibitor, with an IC50 of 900 nM and 700 nM, respectively. MitoBloCK-6 also inhibits Erv2 (IC50=1.4 μM). MitoBloCK-6 can induce Apoptosis via cytochrome c release. MitoBloCK-6 inhibits growth of developing zebrafish motor neurons. MitoBloCK-6 has anticancer activity against liver cancer and leukemia.

In Vitro：MitoBloCK-6 (20 μM, 8 h) induces apoptosis via cytochrome c release in human embryonic stem cells (hESCs)[1]. MitoBloCK-6 (20-40 μM, 72 h) inhibits proliferation of liver cancer cells McA-RH7777 via mitochondrial impairment[2]. MitoBloCK-6 kills leukemia cell lines (OCI-AML2, TEX, Jurkat and NB4) with an IC50 of 5-10 µM[3]. MitoBloCK-6 (0.078-5 μM) increases the differentiation of OCI-AML2 and NB4 cells via inhibition of ALR, as increased surface expression of the myeloid markers CD11b[4]. MitoBloCK-6 results in a significant decrease in the growth and branching of developing zebrafish motor neurons via inhibition of ALR[5].

In Vivo：MitoBloCK-6 (80 mg/kg, i.p., 5 of 7 days, twice daily) reduces tumor growth and the engraftment of AML cells into the marrow in mice xenografted with OCI-AML2 cells[4]. MitoBloCK-6 (80 mg/kg i.p. 5 of 7 days, 2 weeks) strongly reduces the engraftment of primary AML cells in mice[6].

IC50 & Target：IC50: 900 nM (Erv1) 700 nM (ALR) 1.4 μM (Erv2)[1] In Vitro MitoBloCK-6 (20 μM, 8 h) induces apoptosis via cytochrome c release in human embryonic stem cells (hESCs)[1]. MitoBloCK-6 (20-40 μM, 72 h) inhibits proliferation of liver cancer cells McA-RH7777 via mitochondrial impairment[2]. MitoBloCK-6 kills leukemia cell lines (OCI-AML2, TEX, Jurkat and NB4) with an IC50 of 5-10 µM[3]. MitoBloCK-6 (0.078-5 μM) increases the differentiation of OCI-AML2 and NB4 cells via inhibition of ALR, as increased surface expression of the myeloid markers CD11b[4]. MitoBloCK-6 results in a significant decrease in the growth and branching of developing zebrafish motor neurons via inhibition of ALR[5]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> MitoBloCK-6 Related Antibodies Apoptosis Analysis [1] Cell Line: human embryonic stem cells

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References：

[1]. Dabir DV, et, al. A small molecule inhibitor of redox-regulated protein translocation into mitochondria. Dev Cell. 2013 Apr 15;25(1):81-92.  [Content Brief]

[2]. Kabiri Y, et al. Mitochondrial Impairment by MitoBloCK-6 Inhibits Liver Cancer Cell Proliferation. Front Cell Dev Biol. 2021 Sep 20;9:725474.  [Content Brief]

[3]. Jeyaraju D V, et al. Inhibition of the mitochondrial protein import machinery is selectively cytotoxic to acute myeloid leukemia (AML) cells and stem cells. Blood, 2016, 128(22): 1572.

[4]. Singh RP, et al. Disrupting Mitochondrial Copper Distribution Inhibits Leukemic Stem Cell Self-Renewal. Cell Stem Cell. 2020 Jun 4;26(6):926-937.e10.  [Content Brief]

[5]. Johnson M E. One Fish, Two Fish, Small Fish, Huge Fish: Utilizing Zebrafish as a Model for Studying Mitochondrial Function. UCLA, 2012.

[6]. Jeyaraju D V, et al. Inhibiting the Mitochondrial Sulfhydryl Oxidase Alr Reduces Cox17 and Alters Mitochondrial Cristae Structure Leading to the Differentiation of AML and Stem Cells. 2017.