Histrelin
Histrelin, a GnRH analogue, is a GnRH Receptor agonist. Histrelin increases serum luteinising hormone (LH), follicle stimulating hormone (FSH) and testosterone levels. Histrelin can be used in the research of prostate cancer, endometriosis.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 76712-82-8
- 分子式: C66H86N18O12
- 分子量:1323.50
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
IC50 & Target
GnRH Receptor[1]
体外実験
Histrelin (10-100 nM) stimulates the release of vasopressin (VP) from from isolated rat hypothalamo-neurohypophysial explants[4].
Histrelin (100 nM) stimulates oxytocin (OT) release from the rat hypothalamo-neurohypophysial system[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
体内実験
Histrelin (10,30, or 100 μg /day, subcutaneous injection) reduces the number of endometrial glands and atrophied the stroma in rabbits[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Csfmop/Csfmop mice [2]
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Dosage:0.001, 0.05, and 0.1 mg/kg
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Administration:Subcutaneous injection
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Result:Increased serum FSH concentrations by 4-fold.
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Animal Model:Rabbits[3]
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Dosage:10, 30, or 100 μg /day
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Administration:Subcutaneous injection for 4 weeks
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Result:Caused a regression of the endometrial glands and a thinning of the stroma.
化学情報
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CAS 番号 76712-82-8
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分子量 1323.50
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分子式 C66H86N18O12
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配列
{Pyr}-His-Trp-Ser-Tyr-D-His(Bzl)-Leu-Arg-Pro-NHEt
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シーケンスの短縮
{Pyr}-HWSYHLRP-NHEt
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
純度とドキュメンテーション
参考文献
[1]. Emma D Deeks, et al. Histrelin: in advanced prostate cancer. Drugs. 2010 Mar 26;70(5):623-30. [Content Brief]
[2]. P E Cohen, et al. Colony-stimulating factor-1 plays a major role in the development of reproductive function in male mice. Mol Endocrinol. 1997 Oct;11(11):1636-50. [Content Brief]
[3]. D W Hahn, et al. Development of an animal model for quantitatively evaluating effects of drugs on endometriosis. Fertil Steril. 1985 Sep;44(3):410-5. [Content Brief]
[4]. E Boczek-Leszczyk, et al. Vasopressin release from the rat hypothalamo-neurohypophysial system: effects of gonadotrophin-releasing hormone (GnRH), its analogues and melatonin. J Physiol Pharmacol. 2010 Aug;61(4):459-66. [Content Brief]
[5]. Marlena Juszczak, et al. Hypothalamic gonadotropin-releasing hormone receptor activation stimulates oxytocin release from the rat hypothalamo-neurohypophysial system while melatonin inhibits this process. Brain Res Bull. 2010 Jan 15;81(1):185-90. [Content Brief]
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)