rel-Vepdegestrant
(Rac)-Vepdegestrant is the relative configuration of Vepdegestrant (HY-138642). Vepdegestrant is an orally active PROTAC estrogen receptor degrader against breast cancer. Vepdegestrant is a hetero-bifunctional molecule that facilitates the interactions between estrogen receptor alpha and an intracellular E3 ligase complex. Vepdegestrant leads to the ubiquitylation and subsequent degradation of estrogen receptors via the proteasome. Vepdegestrant robustly degrades ER in ER-positive breast cancer cell lines with a half-maximal degradation concentration (DC50) of about 2 nM.
(Pink: ERα Target protein ligand; Blue: Cereblon ligand (HY-138793); Black: linker).
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- CAS No.: 2614417-52-4
- Formule: C45H49N5O4
- Masse moléculaire:723.90
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MCF7 | IC50 |
2.7 nM
Compound: 7; ARV-471
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Antiproliferative activity against human MCF7 cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo reagent based luminescence analysis
Antiproliferative activity against human MCF7 cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo reagent based luminescence analysis
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[PMID: 39610216] |
| MCF7 | IC50 |
133 nM
Compound: 7; ARV-471
|
Antiproliferative activity against human MCF7 cells harboring ER-alpha Y537S mutant assessed as inhibition of cell growth
Antiproliferative activity against human MCF7 cells harboring ER-alpha Y537S mutant assessed as inhibition of cell growth
|
[PMID: 39610216] |
Chemical Information
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CAS No. 2614417-52-4
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Masse moléculaire 723.90
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Formule C45H49N5O4
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SMILES
OC1=CC=C([C@@H](C2=CC=C(N3CCC(CC3)CN4CCN(C5=CC=C(C(N([C@@H]6C(NC(CC6)=O)=O)C7)=O)C7=C5)CC4)C=C2)[C@@H](C8=CC=CC=C8)CC9)C9=C1
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Synonyms
rel-ARV-471; rel-PF-07850327
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
Pureté et documentation
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)