TAK-075
TAK-075 is an orally active CaSR antagonist with an IC50 value of 0.94 nM. TAK-075 can stimulate the transient secretion of parathyroid hormone (PTH) in rats and can effectively prevent a significant reduction in PTH secretion caused by the accumulation of active metabolites, maintaining the normal secretion pattern of PTH. TAK-075 can be used in the research of metabolic diseases and osteoporosis.
For research use only. We do not sell to patients.
- CAS No.: 667931-33-1
- Formula: C36H46N4O4S
- Molecular Weight:630.84
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| CHO | IC50 |
0.94 nM
Compound: 10m, TAK-075
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Antagonist activity at CaSR expressed in CHO cells assessed as inhibition of [35S]GTPgammaS binding after 10 mins by scintillation counting
Antagonist activity at CaSR expressed in CHO cells assessed as inhibition of [35S]GTPgammaS binding after 10 mins by scintillation counting
|
[PMID: 21353570] |
Chemical Information
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CAS No. 667931-33-1
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Molecular Weight 630.84
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Formula C36H46N4O4S
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SMILES
O=S(O)(C1=CC=C(C=C1)C)=O.CCC(CC)(C2=CC=C(C=C2)CC)NC(C3=C4N(N=C3C)C(C)(C[C@H](C5=CC=CC=C5)N4)C)=O
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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)