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Key Documents

J3705

Sigma-Aldrich

JB1 trifluoroacetate salt

≥98% (HPLC)

Sinônimo(s):

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

Fórmula empírica (Notação de Hill):
C55H88N14O15S2 · xC2HF3O2
Número CAS:
Peso molecular:
1249.50 (free base basis)
Número MDL:
Código UNSPSC:
12352200
ID de substância PubChem:
NACRES:
NA.77

Ensaio

≥98% (HPLC)

forma

film

condição de armazenamento

desiccated

Condições de expedição

wet ice

temperatura de armazenamento

−20°C

cadeia de caracteres SMILES

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

chave InChI

MPUVBZQBFGGAAS-XHGDPFBQSA-N

Ações bioquímicas/fisiológicas

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.

Características e benefícios

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

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

nwg

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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Visite a Biblioteca de Documentos

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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