A peptide derivative of human IGF-1
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IGF-1 LR3

Item No. 45532

Technical Information
Synonyms
  • IGF-1 Long Arginine 3
  • Long [Arg3]-IGF-I
  • LR3-IGF-I
Purity
≥95%
A solid
Peptide Sequence
MFPAMPLSSLFVNGPRTLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA-OH
DMSO: Sparingly soluble: 1-10 mg/mlWater: Sparingly soluble: 1-10 mg/ml
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    Product Description

    IGF-1 long arginine 3 (IGF-1 LR3) is a peptide derivative of human insulin-like growth factor 1 (IGF-1; Item No. 33981) containing 13 additional amino acids at the N-terminus of IGF-1 as well as an arginine in place of glutamate at position 3 of IGF-1, a substitution that increases its half-life by reducing its interaction with IGF binding proteins (IGFBPs).1 It stimulates protein and DNA synthesis (EC50s = 0.19 and 1.8 nM, respectively) and prevents protein degradation in vitro (EC50 = 0.53 nM) to a greater degree than IGF-1. IGF-1 LR3 (278 µg/animal per day) increases body weight, muscle RNA content, and muscle protein synthesis in a rat model of diabetes.2 It reduces vessel stenosis and the necrotic core size of atherosclerotic plaques in a model of early atherosclerosis using ApoE-/- mice.3

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Francis, G.L., Ross, M., Ballard, F.J., et alNovel recombinant fusion protein analogues of insulin-like growth factor (IGF)-I indicate the relative importance of IGF-binding protein and receptor binding for enhanced biological potency. J. Mol. Endocrinol. 8(3), 213-223 (1992).

    2. Tomas, F.M., Knowles, S.E., Owens, P.C., et alInsulin-like growth factor-I and more potent variants restore growth of diabetic rats without inducing all characteristic insulin effects. Biochem. J. 291(Pt 3), 781-786 (1993).

    3. von der Thüsen, J.H., Borensztajn, K.S., Moimas, S., et alIGF-1 has plaque-stabilizing effects in atherosclerosis by altering vascular smooth muscle cell phenotype. Am. J. Pathol. 178(2), 924-934 (2011).