aneurysms using RIP1 inhibitors Necrostatin-1 (Nec-1)

biovision nec 1s


A potent necroptosis inhibitor. Displays higher activity in inhibiting necroptosis in Jurkat cells than Nec-1 (Cat. No. 1864) (EC₅₀ = 210 nM versus EC₅₀ = 490 nM), as well as showing no nonspecific cytotoxicity at high concentrations (~100 mM). More useful for in-cell and in vivo experiments compared to Nec-1.

Product Details:

Alternate Name 5-((7-Cl-1H-indol-3-yl)methyl)-3-methylimidazolidine-2,4-dione); 7-Cl-O-Nec-1
Peptide Sequence No
Appearance Yellow solid
CAS # 852391-15-2
Molecular Formula C₁₃H₁₂ClN₃O₂
Molecular Weight 277.71
Purity ≥96% by TLC and LC-MS
Solubility DMSO
InChi InChI=1S/C13H12ClN3O2/c1-17-12(18)10(16-13(17)19)5-7-6-15-11-8(7)3-2-4-9(11)14/h2-4,6,10,15H,5H2,1H3,(H,16,19)
PubChem CID 643953
Handling Protect from light and moisture
Storage Conditions -20°C
Shipping Conditions Gel Pack
USAGE For Research Use Only! Not For Use in Humans.
biovision nec 1s
biovision nec 1s

Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive nature. There is no approved pharmacological treatment that would effectively slow the growth of the aneurysm or prevent rupture. Necrosis is a form of programmed necrosis that is regulated by receptor-interacting protein kinases (RIPs). We have recently shown that a lack of RIP3 in mice prevented aneurysm formation.

The aim of this study is to test whether disruptive necrosis affects the progression of existing aneurysms using RIP1 inhibitors Necrostatin-1 (Nec-1) and optimized forms of Nec-1, 7-Cl-O-Nec-1 (Nec-1 s). Seven days after induction of the aneurysm by elastase perfusion, mice were randomly administered DMSO, Nec-1 (3.2 mg / kg / day) and Nec-1s (1.6 mg / kg / day) by intraperitoneal injection. After sacrifice on day 14 of postaneurysm induction, the aortic expansion in the Nec-1s group (64.12 ± 4.80%) was significantly smaller than in the DMSO group (172.80 ± 13.68%) (P <0.05).

The mean aortic diameter of Nec-1-treated mice appeared to be smaller (121.60 ± 10.40%) than the DMSO group, although the difference was not statistically significant (P = 0.1). Histologically, the aortic structure of Nec-1s-treated mice appeared normal, with continuous and organized elastin layers and rich SMCs expressing αActin.

In addition, Nect-1 treatment reduced macrophage infiltration and MMP9 accumulation and increased tropoelastin and lysyl oxidase aortic levels. Together, our data suggest that pharmacological inhibition of necrosis by Nec-1 stabilizes pre-existing aneurysms by reducing inflammation and promoting connective tissue repair.



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