RET-IN-34
RET-IN-34 is a RET inhibitor with an IC50 of 0.89 nM. RET-IN-34 serves as a target protein ligand for PROTAC synthesis (Ligand for Target Protein for PROTAC). RET-IN-34 is applicable for the synthesis of PROTAC RET Degrader 2 (HY-183783). RET-IN-34 exhibits anticancer activity against medullary thyroid carcinoma. RET-IN-34 can be used in studies related to medullary thyroid carcinoma.
For research use only. We do not sell to patients.
- CAS No.: 2222758-09-8
- Formula: C31H34N8O2
- Molecular Weight:550.65
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
RET-IN-34 (Compound EV1) inhibits RET kinase in a cell-free biochemical assay with an IC50 of 0.89 nM[1].
RET-IN-34 (240 h) inhibits the growth of TT medullary thyroid carcinoma cells with a GI50 of 0.35 μM[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. 2222758-09-8
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Molecular Weight 550.65
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Formula C31H34N8O2
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SMILES
COC1=NC=C(C=C1)CN2C3CC2CN(C3)C4=NC=C(C=C4)C5=CC(OCC6CCNCC6)=CN7N=CC(C#N)=C57
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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)