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Merck

J3705

Sigma-Aldrich

JB1 trifluoroacetate salt

≥98% (HPLC)

Sinónimos:

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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1 MG
MXP 3,725.00

MXP 3,725.00


Fecha estimada de envío26 de abril de 2025



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1 MG
MXP 3,725.00

About This Item

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

MXP 3,725.00


Fecha estimada de envío26 de abril de 2025


Nivel de calidad

Ensayo

≥98% (HPLC)

Formulario

film

condiciones de almacenamiento

desiccated

Condiciones de envío

wet ice

temp. de almacenamiento

−20°C

cadena 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

Clave InChI

MPUVBZQBFGGAAS-XHGDPFBQSA-N

Acciones bioquímicas o fisiológicas

JB1 is an IGF-I peptide analog; IGF-1 receptor antagonist.
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 y beneficios

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 clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

nwg

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


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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
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
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
Andrew Sunters et al.
The Journal of biological chemistry, 285(12), 8743-8758 (2010-01-01)
The capacity of bones to adjust their mass and architecture to withstand the loads of everyday activity derives from the ability of their resident cells to respond appropriately to the strains engendered. To elucidate the mechanisms of strain responsiveness in

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