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Cat. No.: HY-182383

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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.

연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.

CAS No.: 1209002-42-5
화학식: C₃₃H₄₀ClN₉O₄S
분자량:694.25

보관:

Please store the product under the recommended conditions in the Certificate of Analysis.

VMY-1-101 Chemical Structure

CAS No.: 1209002-42-5

Amount: USD 0.00

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- 제품 설명
- Cellular Effect
- In Vitro
Chemical Information
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

All CDK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
MCF7	IC₅₀	19.05 μM Compound: VMY-1-101	Antiproliferative activity against human MCF7 cells expressing estrogen receptor after 48 hrs by WST-1 assay Antiproliferative activity against human MCF7 cells expressing estrogen receptor after 48 hrs by WST-1 assay	[PMID: 21440449]

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.

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.

Related Protocols :

Chemical Information

CAS No. 1209002-42-5
분자량 694.25
화학식 C₃₃H₄₀ClN₉O₄S
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
선적

Room temperature in continental US; may vary elsewhere.
보관

Please store the product under the recommended conditions in the Certificate of Analysis.

순도&문서

Handling Instructions (2659 KB)

References

[1]. Yenugonda VM, et al. Fluorescent cyclin-dependent kinase inhibitors block the proliferation of human breast cancer cells. Bioorg Med Chem. 2011;19(8):2714-2725. [Content Brief]

Calculators

몰농도 계산기

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

농도 희석 계산기

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Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Bioz

Keywords

MOQ

Minimum order quantity

100 mg

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