Alagebrium chloride (ALT711) |
Catalog No.GC33761 |
Alagebrium chloride (ALT711) (ALT711) is an advanced glycation end product (AGE) inhibitor.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 341028-37-3
Sample solution is provided at 25 µL, 10mM.
Alagebrium chloride is an advanced glycation end product (AGE) inhibitor.
Alagebrium chloride is an advanced glycation end product (AGE) inhibitor. Endothelial cell (EC) proliferation is increased for all groups receiving Alagebrium (ALT-711), particularly when seeded on matrix from the AAo of obese (ZO) and diabetic (ZD) rats[2].
Blood pressure is not affected by treatment with Alagebrium. In diabetic RAGE apoE double-KO mice, treatment with Alagebrium is associated with a modest reduction in renal mass and reduces hyperfiltration compare with nontreated mice. Treatment with Alagebrium in diabetic RAGE apoE double-KO mice is associated with a further reduction in glomerular collagen IV levels, approaching levels observed in control mice[1]. Body weight, heart rate (HR), and mean blood pressure (BP) are similar in Zucker lean (ZL), obese (ZO), and diabetic (ZD) groups in the absence or presence of Alagebrium (ALT-711). Alagebrium increases blood flow (BF) in ZO rats but reduces distal vascular resistance in ZD rats. A decrease in neointimal hyperplasia (NH) intrastrut thickness as a function of local radius is found in all groups with Alagebrium treatment. A significant increase in TGF-β expression is also found in the AAo of ZL rats treated with Alagebrium[2].
[1]. Watson AM, et al. Alagebrium reduces glomerular fibrogenesis and inflammation beyond preventing RAGEactivation in diabetic apolipoprotein E knockout mice. Diabetes. 2012 Aug;61(8):2105-13. [2]. Wang H, et al. Alagebrium inhibits neointimal hyperplasia and restores distributions of wall shear stress by reducing downstream vascular resistance in obese and diabetic rats. Am J Physiol Heart Circ Physiol. 2015 Oct;309(7):H1130-40.
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