IACS-56676
IACS-56676 is a selective NRASG12D inhibitor with a target IC50 of 0.031 μM. IACS-56676 stabilizes the p-loop, maintains key interactions with Asp12, Gly60 and Asp69, and achieves selectivity against wild-type KRAS through substitution targeting Leu95. IACS-56676 can be used in the research of melanoma, hematologic malignancies and thyroid cancer.
For research use only. We do not sell to patients.
- CAS No.: 3105153-34-9
- Formula: C28H28ClF4N5O
- Molecular Weight:562.00
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
IACS-56676 potently reduces viability of NRASG12D-mutant THP1 cells with an IC50 of 0.073 μM[1].
IACS-56676 has minimal CYP inhibition activity, with no measurable inhibition of CYP2D6 and CYP2C9 up to 10 μM, and weak inhibition of CYP3A4 isoforms[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 3105153-34-9
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Molecular Weight 562.00
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Formula C28H28ClF4N5O
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SMILES
NC1=CC(C2=C(F)C(N(C3CC3)C(CNC(C)=O)=C4[C@@]5([H])[C@@]6([H])[C@]5([H])CNC6)=C4C(C7CC7)=N2)=C(C(F)(F)F)C(Cl)=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)