2. JAK/STAT Signaling Protein Tyrosine Kinase/RTK Apoptosis Cell Cycle/DNA Damage
  3. EGFR Apoptosis DNA/RNA Synthesis
  4. EGFR-IN-210

EGFR-IN-210 is a EGFR kinase inhibitor with an IC50 of 0.198 μM. EGFR-IN-210 induces antiproliferative, pro-apoptotic, G0/G1 cell cycle arrest, DNA synthesis inhibition and anti-migratory effects in cancer cells. EGFR-IN-210 can be used for the research of various cancers including colorectal cancer.

For research use only. We do not sell to patients.

EGFR-IN-210

EGFR-IN-210 Chemical Structure

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EGFR-IN-210 Related Antibodies

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Description

EGFR-IN-210 is a EGFR kinase inhibitor with an IC50 of 0.198 μM. EGFR-IN-210 induces antiproliferative, pro-apoptotic, G0/G1 cell cycle arrest, DNA synthesis inhibition and anti-migratory effects in cancer cells. EGFR-IN-210 can be used for the research of various cancers including colorectal cancer[1].

In Vitro

EGFR-IN-210 (Compound T6) exhibits broad-spectrum antiproliferative activity in the NCI-60 cell panel, with an average growth inhibition rate exceeding 100% across 5 cancer subtypes and a maximum inhibition rate of up to 200% in individual sensitive cell lines[1].
EGFR-IN-210 (0.53 μM; 48 h) potently inhibits the migration of HT29 colon cancer cells, reducing the wound healing rate to 16.85% within 48 h[1].
EGFR-IN-210 (0.53 μM; 1-3 weeks) potently inhibits the long-term proliferation and colony-forming abilities of HT29 colorectal cancer cells[1].
EGFR-IN-210 (0.53 μM; 24 h) induces G0/G1 cell cycle arrest in HT29 colorectal cancer cells, reduces the proportion of S-phase cells, while maintaining G2/M-phase cell levels comparable to those of the untreated control group[1].
EGFR-IN-210 (0.53 μM; 24 h) induces significant apoptosis in HT29 colorectal cancer cells, with a total apoptosis rate of 67.40%, and this process is mainly mediated via the late apoptosis pathway[1].
EGFR-IN-210 (48 h) exhibits favorable in vitro safety profiles, with low cytotoxicity against normal WI-38 human lung fibroblasts (IC50: 156.59 μM)[1].

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

EGFR-IN-210 Related Antibodies

Cell Migration Assay [1]

Cell Line: HT29 colorectal cancer cells
Concentration: 0.53 μM (IC50 concentration)
Incubation Time: 48 h
Result: Potently inhibited HT29 colorectal cancer cell migration, reducing wound closure to 16.85% over 48 h.

Cell Cycle Analysis[1]

Cell Line: HT29 colorectal cancer cells
Concentration: 0.53 μM (IC50 concentration)
Incubation Time: 24 h
Result: Induced G0/G1 cell cycle arrest, with 84.56% of cells in G0/G1 phase, 12.95% in S phase, and 1.97% in G2/M phase, compared to 82.58% (G0/G1), 15.45% (S), and 1.97% (G2/M) in untreated controls.

Apoptosis Analysis[1]

Cell Line: HT29 colorectal cancer cells
Concentration: 0.53 μM (IC50 concentration)
Incubation Time: 24 h
Result: Increased total apoptosis to 67.40%, consisting of 5.67% early apoptosis and 61.73% late apoptosis, compared to 30.16% total apoptosis (9.76% early, 20.40% late) in untreated controls.
Increased necrosis to 19.82%, compared to 3.89% in controls.
Molecular Weight

630.14

Formula

C30H24ClN7O3S2
SMILES

O=C1N(CC2=CC=CC=C2)C(SCC3=CN(CC(NC4=NC=C(C5=CC=C(OC)C=C5)S4)=O)N=N3)=NC6=CC(Cl)=CC=C61
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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EGFR-IN-210 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:

EGFR-IN-210EGFRApoptosisDNA/RNA SynthesisEpidermal growth factor receptorErbB-1HER1breast cancerprostate cancerEGFR kinasemelanomanon-small cell lung cancercolorectal cancerCNS cancerovarian cancerrenal cancercancer cellsInhibitorinhibitorinhibit

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