NTU281

Modify Date: 2024-09-11 18:46:48

NTU281 Structure
NTU281 structure
Common Name NTU281
CAS Number 815619-12-6 Molecular Weight 487.59
Density N/A Boiling Point N/A
Molecular Formula C25H31N2O6S+ Melting Point N/A
MSDS N/A Flash Point N/A

 Use of NTU281


NTU281 is a potent transglutaminase-2 inhibitor. NTU281 can reduce the increases in serum creatinine and albuminuria in diabetic rats. NTU281 can also reduce glomerular collagen I accumulation, Hic-5 and α-SMA expression, and apoptosis. NTU281 can be used for researching glomerulosclerosis caused by diabetes[1][2].

 Names

Name NTU281

 NTU281 Biological Activity

Description NTU281 is a potent transglutaminase-2 inhibitor. NTU281 can reduce the increases in serum creatinine and albuminuria in diabetic rats. NTU281 can also reduce glomerular collagen I accumulation, Hic-5 and α-SMA expression, and apoptosis. NTU281 can be used for researching glomerulosclerosis caused by diabetes[1][2].
Related Catalog
In Vivo NTU281 (2.5 μl/h of 50 mM; cannulate to deliver into kidneys) reduces glomerular collagen I overexpression as well as the increases in glomerular Hic-5 and α-SMA expression; also decreases serum creatinine, albuminuria, glomerulosclerosis and tubulointerstitial scarring in diabetic rats[1][2]. Animal Model: Male Wistar Han rats [subjected to right uninephrectomy, then induced hyperglycemia by tail vein injection of streptozotocin (35 mg/kg in citrate buffer pH 4)][1] Dosage: 2.5 μl/h of 50 mM Administration: Cannulated to deliver into kidneys Result: Reduced glomerular collagen I overexpression by ~50%; reduced the increases in glomerular Hic-5 expression; reduced diabetic nephropathy-induced α-SMA expression. Animal Model: Male Wistar Han rats [subjected to right uninephrectomy, then induced hyperglycemia by tail vein injection of streptozotocin (35 mg/kg in citrate buffer pH 4)][2] Dosage: Various concentration Administration: Cannulated to deliver into kidneys Result: Significantly reduced the increases in serum creatinine (-68%) and albuminuria (-80%) in diabetic rats during eight-month experimental period; reduced in glomerulosclerosis (-76.6%) and tubulointerstitial scarring (-68.2%) as a result of lowered accumulation of collagen I, III and IV; and reduced numbers of myofibroblasts present.
References

[1]. Hornigold N, et al. Inhibition of collagen I accumulation reduces glomerulosclerosis by a Hic-5-dependent mechanism in experimental diabetic nephropathy. Lab Invest. 2013 May;93(5):553-65.

[2]. Huang L, et al. Do changes in transglutaminase activity alter latent transforming growth factor beta activation in experimental diabetic nephropathy? Nephrol Dial Transplant. 2010 Dec;25(12):3897-910.

 Chemical & Physical Properties

Molecular Formula C25H31N2O6S+
Molecular Weight 487.59