2. Cell Cycle/DNA Damage Apoptosis
  3. CDK Apoptosis
  4. VMY-1-101

VMY-1-101 is a fluorescent cyclin-dependent kinase (CDK) inhibitor, with an excitation of 410 nm and emission of 512 nm. VMY-1-101 competitively inhibits ATP binding to CDKs. VMY-1-101 induces G2/M cell cycle arrest in human breast cancer cells. VMY-1-101 induces modest apoptosis in human breast cancer cells. VMY-1-101 blocks proliferation of human breast cancer cells, including multidrug resistance-positive cells, and is not a substrate for p-glycoprotein. VMY-1-101 localizes to the cytoplasm of human breast cancer cells. VMY-1-101 shows increased binding to human breast cancer tissue compared to fluorophore alone. VMY-1-101 can be used for the research of breast cancer.

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VMY-1-101

VMY-1-101 Chemical Structure

CAS No. : 1209002-42-5

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VMY-1-101 Related Antibodies

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Description

VMY-1-101 is a fluorescent cyclin-dependent kinase (CDK) inhibitor, with an excitation of 410 nm and emission of 512 nm. VMY-1-101 competitively inhibits ATP binding to CDKs. VMY-1-101 induces G2/M cell cycle arrest in human breast cancer cells. VMY-1-101 induces modest apoptosis in human breast cancer cells. VMY-1-101 blocks proliferation of human breast cancer cells, including multidrug resistance-positive cells, and is not a substrate for p-glycoprotein. VMY-1-101 localizes to the cytoplasm of human breast cancer cells. VMY-1-101 shows increased binding to human breast cancer tissue compared to fluorophore alone. VMY-1-101 can be used for the research of breast cancer[1].

In Vitro

VMY-1-101 (0.1 μM; 40 min) most potently inhibits the CDK2/cyclin E complex (87% inhibition) among tested purified human CDK/cyclin complexes, with varying degrees of inhibition across other CDK isoforms[1].
VMY-1-101 (1-100 μM; 48 h) potently inhibits the proliferation of human MDA-MB-231 breast cancer cells (IC50 = 4.86 μM) and MCF-7 breast cancer cells (IC50 = 19.05 μM) in a 48-h WST-1 assay[1].
VMY-1-101 (5-10 μM; 16 h, 24 h, 40 h) induces G2/M phase cell cycle arrest and moderate cell death in human MDA-MB-231 and MCF-7 breast cancer cells after 16 h, 24 h, or 40 h of treatment[1].
VMY-1-101 (10 μM; 48 h) reduces cell density and induces aberrant morphological changes in human MDA-MB-231 and MCF-7 breast cancer cells[1].
VMY-1-101 (10 μM; 48 h, 72 h) induces apoptotic signaling in human MDA-MB-231 breast cancer cells by altering Bcl-2/Bax protein levels and promoting PARP cleavage[1].
VMY-1-101 (10 μM; 24 h) induces significant early and late apoptosis in human MCF-7 breast cancer cells[1].

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

VMY-1-101 Related Antibodies

Cell Cycle Analysis[1]

Cell Line: human MDA-MB-231 breast cancer cells, human MCF-7 breast cancer cells
Concentration: 5 μM; 10 μM
Incubation Time: 16 h, 24 h, 40 h
Result: Induced a clear accumulation of cells in the G2/M phase in both MDA-MB-231 and MCF-7 cells at both 5 μM and 10 μM after 24 h.
Induced similar G2/M phase accumulation patterns at 16 h and 40 h.
Detected a moderate increase in sub-G1 cells (indicating cell death).

Western Blot Analysis[1]

Cell Line: human MDA-MB-231 breast cancer cells
Concentration: 10 μM
Incubation Time: 48 h
Result: Reduced the level of anti-apoptotic Bcl-2 protein after 48 h of treatment.
Increased the level of pro-apoptotic Bax protein after 48 h of treatment, shifting the balance toward apoptosis.

Western Blot Analysis[1]

Cell Line: human MDA-MB-231 breast cancer cells
Concentration: 10 μM; 20 μM; 40 μM
Incubation Time: 72 h
Result: Promoted moderate cleavage of the 116 kDa full-length PARP protein into an 89 kDa fragment, a marker of apoptotic signaling, after 72 h of treatment.

Apoptosis Analysis[1]

Cell Line: human MCF-7 breast cancer cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Provoked a significant induction of early and late apoptotic cells, as indicated by increased annexin V-positive staining, relative to control cells.
Molecular Weight

694.25

Formula

C33H40ClN9O4S
CAS No.
SMILES

CC(C)N1C2=NC(N[C@@H](CO)CC)=NC(NC3=CC(Cl)=C(C=C3)C(NCCNS(=O)(C4=CC=CC5=C4C=CC=C5N(C)C)=O)=O)=C2N=C1
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Purity & Documentation
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VMY-1-101 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:

VMY-1-1011209002-42-5CDKApoptosisCyclin dependent kinaseG2/M cell cycle arrestATPMCF-7 breast cancer cellsmultidrug resistance-positive cellsp-glycoproteincyclin-dependent kinaseMDA-MB-231 breast cancer cellshuman breast cancer cellsCDK2/cyclin E complexCDKsInhibitorinhibitorinhibit

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