NK3R antagonist-1
NK3R antagonist-1 is an orally active neurokinin-3 receptor (NK3R) antagonist with an IC50 of 53.61 nM. NK3R antagonist-1 reduces plasma luteinizing hormone (LH) levels in ovariectomized rat models. NK3R antagonist-1 is applicable to research related to menopausal hot flushes.
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
- 화학식: C20H18FN5OS
- 분자량:395.45
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
IC50 & Target
[1]|
NK3R 53.61 nM (IC50) |
In Vitro
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (male, 8-12 weeks old, ovariectomized)[1]
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Dosage:120 mg/kg
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Administration:i.g.; single dose
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Result:Significantly reduced plasma luteinizing hormone (LH) levels, with inhibitory effect evident at 45 min post-dose, and statistically significant differences relative to vehicle control observed at both 45 and 90 min post-dose.
Chemical Information
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분자량 395.45
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화학식 C20H18FN5OS
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SMILES
CC1=NSC(C2=NC(C#CC)=C([C@H]3C)N2CCN3C(C4=CC=C(F)C=C4)=O)=N1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)