2. Protein Tyrosine Kinase/RTK Autophagy Apoptosis
  3. VEGFR Autophagy Apoptosis
  4. Coibamide A

Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, shows potent antiproliferative activity. Coibamide A induces autophagosome accumulation via an mTOR-independent mechanism. Coibamide A induces apoptosis. Coibamide A inhibits VEGFA/VEGFR2 expression and suppresses tumor growth in glioblastoma xenografts.

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Coibamide A Chemical Structure

Coibamide A Chemical Structure

CAS No. : 1029227-48-2

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Coibamide A Related Antibodies

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Description

Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, shows potent antiproliferative activity. Coibamide A induces autophagosome accumulation via an mTOR-independent mechanism. Coibamide A induces apoptosis. Coibamide A inhibits VEGFA/VEGFR2 expression and suppresses tumor growth in glioblastoma xenografts[1][2].

IC50 & Target[2]

VEGFR2

 

In Vitro

Coibamide A (0.3-1 nM; 3-60 hours) inhibits proliferation of MDA-MB-231 breast cancer cells[1].
Coibamide A (2.3-230 nM; 3 days) produces concentration- and time-dependent cell death in human U87-MG and SF-295 glioblastoma cells[2].
Coibamide A (10-300 nM; 72 h) induces activation of caspase-3/7 and apoptosis in a cell type-specific manner[2].
Coibamide A (20 nM; 48 h) induces autophagosome accumulation in apoptotic-resistant U87-MG cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Coibamide A Related Antibodies

Cell Proliferation Assay[1]

Cell Line: MDA-MB-231 breast cancer cells
Concentration: 0.3, 1 nM
Incubation Time: 3-60 hours
Result: Showed a steady concentration-dependent decrease in proliferative activity relative to vehicle-treated cells

Cell Cytotoxicity Assay[2]

Cell Line: U87-MG and SF-295 cells
Concentration: 2.3 to 230 nM
Incubation Time: 3 days
Result: Induced concentration-dependent cytotoxicity with EC50 values of 28.8 nM and 96.2 nM for U87-MG and SF-295 cells, respectively.

Apoptosis Analysis[2]

Cell Line: U87-MG and SF-295 cells
Concentration: 10-300 nM
Incubation Time: 72 h
Result: An 89 kDa band corresponding to the caspase 3-cleaved form of PARP1 was readily detected by 48 h indicative of apoptotic cell death in SF-295 cells, whereas only trace levels of this fragment were observed in late, detaching U87-MG cell lysates

Cell Autophagy Assay[2]

Cell Line: U87-MG cell
Concentration: 20 nM
Incubation Time: 48 h
Result: Caused a clear increase in LC3-II expression by 1 h, and this increase in LC3-II expression was generally sustained through 48 h.
In Vivo

Coibamide A (300 μg/kg; intratumoral injections; for the first two days, and then every 48 h afterward for 35 days) inhibits tumor growth in a subcutaneous mouse model of glioblastoma[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: 8-week old female nude athymic mice with U87-MG cells[1]
Dosage: 300 μg/kg
Administration: Intratumoral injections; for the first two days, and then every 48 h afterward for 35 days
Result: Remained stable at 200-300 mm3 without significant growth over 4 weeks of treatmen, whereas the tumors of vehicle-treated animals continued to grow at a steady rate consistent with this aggressive cancer cell type
Molecular Weight

1287.63

Formula

C65H110N10O16
CAS No.
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References
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Coibamide A Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Coibamide A1029227-48-2VEGFRAutophagyApoptosisVascular endothelial growth factor receptorN-methyl-stabilizedcytotoxicdepsipeptideantiproliferativeautophagosomemTORVEGFA/VEGFR2glioblastoma xenograftInhibitorinhibitorinhibit

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