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Merck

J3705

Sigma-Aldrich

JB1 trifluoroacetate salt

≥98% (HPLC)

别名:

H-Cys-Tyr-Ala-Ala-Pro-Leu-Lys-Pro-Ala-Lys-Ser-Cys-OH trifluoroacetate salt, JB-1 trifluoroacetate salt, L-Cysteinyl-L-tyrosyl-L-alanyl-L-alanyl-L-prolyl-L-leucyl-L-lysyl-L-prolyl-L-alanyl-L-lysyl-L-seryl-L-Cysteine, cyclic (1-12)-disulfide trifluoroacetate salt

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About This Item

经验公式(希尔记法):
C55H88N14O15S2 · xC2HF3O2
分子量:
1249.50 (free base basis)
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77

品質等級

化驗

≥98% (HPLC)

形狀

film

儲存條件

desiccated

運輸包裝

wet ice

儲存溫度

−20°C

SMILES 字串

CC(C)C[C@@H]1NC(=O)[C@@H]2CCCN2C(=O)[C@H](C)NC(=O)[C@H](C)NC(=O)[C@H](Cc3ccc(O)cc3)NC(=O)[C@@H](N)CSSC[C@H](NC(=O)[C@H](CO)NC(=O)[C@H](CCCCN)NC(=O)[C@H](C)NC(=O)[C@@H]4CCCN4C(=O)[C@H](CCCCN)NC1=O)C(O)=O

InChI

1S/C55H88N14O15S2/c1-29(2)24-38-49(77)63-37(13-7-9-21-57)54(82)69-23-11-14-42(69)51(79)60-31(4)45(73)62-36(12-6-8-20-56)47(75)66-40(26-70)50(78)67-41(55(83)84)28-86-85-27-35(58)46(74)64-39(25-33-16-18-34(71)19-17-33)48(76)59-30(3)44(72)61-32(5)53(81)68-22-10-15-43(68)52(80)65-38/h16-19,29-32,35-43,70-71H,6-15,20-28,56-58H2,1-5H3,(H,59,76)(H,60,79)(H,61,72)(H,62,73)(H,63,77)(H,64,74)(H,65,80)(H,66,75)(H,67,78)(H,83,84)/t30-,31-,32-,35-,36-,37-,38-,39-,40-,41-,42-,43-/m0/s1

InChI 密鑰

MPUVBZQBFGGAAS-XHGDPFBQSA-N

生化/生理作用

JB1 is an IGF-I peptide analog; IGF-1 receptor antagonist. IGF-1, once known as somatomedin C, is involved in a multitude of activites including promoting growth and development, particularly neural development, and involved in the growth and proliferation in a variety of human cancers. JB1 is a 12-amino acid cyclic peptide, an IGF-1 analog, used by researchers in a variety of fields to inhibit IGF activity by inhibiting binding of IGF-1 to its receptor.

特點和優勢

This compound is featured on the InsR page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

nwg

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Jun Ren et al.
Cardiovascular research, 57(3), 738-748 (2003-03-06)
Cardiac resistance to IGF-1 occurs in diabetes and is attributed to cardiac dysfunction in diabetes. However, the mechanism of action responsible for cardiac IGF-1 resistance is still unknown. This study was designed to examine the impact of high glucose on
Feng Dong et al.
American journal of physiology. Heart and circulatory physiology, 289(1), H78-H84 (2005-03-01)
Hearts from severely Cu-deficient rats show a variety of pathological defects, including hypertrophy and, in intact hearts, depression of contractile function. Paradoxically, isolated cardiomyocytes from these rats exhibit enhanced contractile properties. Because hypertrophy and enhanced contractility observed with other pathologies
J Ren
Cardiovascular research, 46(1), 162-171 (2000-03-23)
Insulin-like growth factor I (IGF-1) stimulates cardiac growth and contraction, but resistance to its action has been reported in diabetes. This study was to determine if IGF-1-induced cardiac contractile action is altered in rats genetically predisposed to diabetes. Ventricular myocytes
M van Eickels et al.
British journal of pharmacology, 131(8), 1592-1596 (2001-01-05)
The effects of angiotensin-converting enzyme (ACE) inhibition and angiotensin type 1 (AT(1)) receptor blockade on insulin-like growth factor-I (IGF-I) induced proliferation and immediate-early-gene expression of neonatal rat cardiac fibroblasts were investigated. Moreover the role of the IGF-I receptor (IGF-IR) in
Kadon K Hintz et al.
Diabetes research and clinical practice, 55(2), 89-98 (2002-02-14)
Resistance to insulin-like growth factor I (IGF-1)-induced cardiac contractile response has been reported in diabetes. To evaluate the role of prediabetic insulin resistance to cardiac IGF-1 resistance, whole body insulin resistance was generated with dietary sucrose and contractile function was

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