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Merck
CN

L6524

Sigma-Aldrich

[D-pGlu1, D-Phe2, D-Trp3,6]-LH-RH

≥97% (HPLC)

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关于此项目

经验公式（希尔记法）:
C67H84N16O13
化学文摘社编号:
68059-94-9
分子量:
1321.48
MDL编号:
MFCD00076582
UNSPSC代码:
12352200

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方案

≥97% (HPLC)

储存温度

−20°C

SMILES字符串

CC(C)C[C@H](NC(=O)[C@@H](Cc1c[nH]c2ccccc12)NC(=O)[C@H](Cc3ccc(O)cc3)NC(=O)[C@H](CO)NC(=O)[C@@H](Cc4c[nH]c5ccccc45)NC(=O)[C@@H](Cc6ccccc6)NC(=O)[C@H]7CCC(=O)N7)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N8CCC[C@H]8C(=O)NCC(N)=O

InChI

1S/C67H84N16O13/c1-37(2)28-49(59(89)76-48(18-10-26-71-67(69)70)66(96)83-27-11-19-55(83)65(95)74-35-56(68)86)77-62(92)52(31-40-33-72-45-16-8-6-14-43(40)45)80-61(91)51(30-39-20-22-42(85)23-21-39)79-64(94)54(36-84)82-63(93)53(32-41-34-73-46-17-9-7-15-44(41)46)81-60(90)50(29-38-12-4-3-5-13-38)78-58(88)47-24-25-57(87)75-47/h3-9,12-17,20-23,33-34,37,47-55,72-73,84-85H,10-11,18-19,24-32,35-36H2,1-2H3,(H2,68,86)(H,74,95)(H,75,87)(H,76,89)(H,77,92)(H,78,88)(H,79,94)(H,80,91)(H,81,90)(H,82,93)(H4,69,70,71)/t47-,48+,49+,50-,51+,52-,53-,54+,55+/m1/s1

InChI key

NYWIVATZZKIKCF-FKDXDCHSSA-N

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Amino Acid Sequence

D-pGlu-D-Phe-D-Trp-Ser-Tyr-D-Trp-Leu-Arg-Pro-Gly-NH2

生化/生理作用

Substance P antagonist; inhibits spinal cord vasomotor responses

其他说明

Similar to L 2636, but produced by Sigma.

象形图

Health hazard
GHS08

警示用语：

Danger

危险声明

H360

危险分类

Repr. 1B

储存分类代码

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type P3 (EN 143) respirator cartridges

法规信息

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分析证书(COA)

Lot/Batch Number

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V Papadopoulos et al.
FEBS letters, 202(1), 74-78 (1986-06-23)
The effects of spent media from seminiferous tubules (STM) on Percoll-purified rat Leydig cells were investigated. Intracellular and extracellular cyclic AMP (cAMP) accumulation and testosterone production were measured. After a 5 h incubation period, STM reduces both the basal and
G Verhoeven et al.
Molecular and cellular endocrinology, 34(1), 7-16 (1984-01-01)
The effects of luteinizing hormone-releasing hormone (LHRH) and an agonistic analogue (LHRHa) have been examined in freshly isolated prepubertal rat interstitial cells and in cells precultured for 6 days in the presence or absence of luteinizing hormone (LH). C19-steroid output
Y Takano et al.
Brain research, 337(2), 357-361 (1985-07-01)
Intrathecal injections of the luteinizing hormone-releasing hormone (LH-RH) analogue, [D-pGlu1-D-Phe2-D-Trp3,6]-LH-RH caused dose-dependent decreases in mean arterial blood pressure in anesthetized rats similar to those seen with [D-Pro4-D-Trp7,9]-substance P4-11. Similarly, intrathecal injections of either peptide reversed the pressor response elicited by
T Funabashi et al.
Endocrine journal, 41(5), 559-563 (1994-10-01)
To gain a better understanding of the existence of an ultra-short feedback mechanism controlling LHRH secretion in the medial preoptic area (MPO), we examined the effects of microinjections of LHRH or the LHRH antagonist [D-pGlu1, D-Phe2, D-Try3,6] into the MPO
M S Blank et al.
Neuroendocrinology, 35(5), 309-312 (1982-11-01)
Administration of a gonadotropin-releasing hormone (GnRH) antagonist, [D-Phe, D-Trp3.6]-GnRH, to immature female rats blocks the equivalent elevations in serum luteinizing hormone (LH) which are provoked by exogenous, natural GnRH (8 ng/100 g BW) or naloxone (0.25 mg/100 g BW), a
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