This is a bulk discount for 10 vials of IGF-2 Lr3 (receptor grade) 10 vials (total 1200mg).
IGF-2 LR3, also called IGF-2 long arginine, and IGF-2 long R3, is a modified synthetic version of the endogenous growth factor insulin-like growth factor 2. Like insulin-like growth factor 1 (IGF-1) and relaxin, IGF-2 shares structural and other similarities to insulin. IGF-2 binds to both the IGF-1 and IGF-2 receptor, displaying an agonistic relationship in the former case and in the latter acting as a signaling antagonist for IGF-1 receptor activity. The “long arginine” modification allows IGF-2 LR3, like IGF-1 LR3, to survive longer in plasma.
The IGF-2 gene is heritable only from the father and is epigenetically imprinted, being heavily influenced by methylation and histone modification.Supraphysiological levels of IGF-2 appear to cause hypoglycemia, which is also the mechanism behind Doege-Potter syndrome (when IGF-2 is overproduced by tumor cells).
Chu et al (2005) find IGF-2 may be useful in preventing myocardial apoptosis following heart failure:
Our results revealed that IGF-II synergistically increased the cell apoptosis induced by suppressing of IGF-IR in neonatal rat ventricular myocytes. After binding of Leu27IGF-II, IGF-IIR became associated with alpha-q polypeptide, acted like a protein-coupled receptor to activate calcineurin, led to the translocation of Bad into mitochondria and release of cytochrome c into cytoplasm, and contributed to mitochondrial-dependent apoptosis in neonatal rat ventricular myocytes. Furthermore, inhibition of IGF-IIR, alpha-q polypeptide, or calcineurin by RNA interference could block the Leu27IGF-II-induced cell apoptosis. Together, this study provides a new insight into the effects of the IGF-IIR and its downstream signaling in myocardial apoptosis. Suppression of IGF-IIR signaling pathways may be a good strategy for both the protection against myocardial cell apoptosis and the prevention of heart failure progression.
Thus far IGF-2 appears to be most active and important during development, but Tong et al (2009) speculate that, since IGF-1 and IGF-2 resistance may be a mechanism of dementia, IGF-1 and IGF-2 may be useful in treating or slowing dementia or related neurodegenerative disorders.
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Tong M, Dong M, de la Monte SM. Brain insulin-like growth factor and neurotrophin resistance in Parkinson's disease and dementia with Lewy bodies: potential role of manganese neurotoxicity. J Alzheimers Dis. 2009 Mar;16(3):585-99.