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品質等級
化驗
≥95% (HPLC)
形狀
film
儲存條件
desiccated
顏色
colorless
運輸包裝
wet ice
儲存溫度
−20°C
InChI
1S/C40H55N7O11S/c1-24(2)19-28(37(55)45-27(36(41)54)17-18-59-4)44-33(49)23-42-39(57)31(21-26-13-9-6-10-14-26)47(3)40(58)30(20-25-11-7-5-8-12-25)46-38(56)29(22-35(52)53)43-32(48)15-16-34(50)51/h5-14,24,27-31H,15-23H2,1-4H3,(H2,41,54)(H,42,57)(H,43,48)(H,44,49)(H,45,55)(H,46,56)(H,50,51)(H,52,53)/t27-,28-,29-,30-,31-/m0/s1
InChI 密鑰
HMHYXLVEFVGOPM-QKUYTOGTSA-N
Amino Acid Sequence
Suc-Asp-Phe-MePhe-Gly-Leu-Met-NH2 trifluoroacetate salt
生化/生理作用
Senktide is a selective Neurokinin NK3 tachykinin receptor agonist. Neurokinins (tachykinins) are members of a family of at least three neuropeptides, substance P, neurokinin A, and neurokinin B (NKB), with each mediating their biological effects through binding to a preferred G-protein-coupled receptor termed NK1, NK2, or NK3, respectively. All three NK receptors are expressed in regions of the central nervous system that are related to emotion and cognition (i.e., amygdala and hippocampus) and have been linked to various degrees in psychiatric disorders. Neurokinin receptors, including NK3 receptors, are also expressed in the motor and sensory systems of the digestive tract.
Senktide treatment in follicular phase goats enhances the liberation of luteinizing hormone (LH) and advance the time of ovulation. Senktide has the ability to suppress gonadotropin-releasing hormone (GnRH) transcription. Treatment with senktide stimulates c-Fos and improve activator protein-1 (AP-1) activity.
儲存類別代碼
11 - Combustible Solids
水污染物質分類(WGK)
WGK 3
閃點(°F)
Not applicable
閃點(°C)
Not applicable
Neurokinin B Causes Acute GnRH Secretion and Repression of GnRH Transcription in GT1?7 GnRH Neurons.
Molecular Endocrinology, 27(3), 437-454 (2013)
Ovarian and hormonal responses to single or continuous peripheral administration of senktide, a neurokinin 3 receptor agonist, during the follicular phase in goats.
Domestic Animal Endocrinology, 53, 136-143 (2015)
Endocrinology, 155(7), 2589-2601 (2014-04-09)
Acute systemic stress disrupts reproductive function by inhibiting pulsatile gonadotropin secretion. The underlying mechanism involves stress-induced suppression of the GnRH pulse generator, the functional unit of which is considered to be the hypothalamic arcuate nucleus kisspeptin/neurokinin B/dynorphin A neurons. Agonists
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