Alternative name

5 – ((7-Cl-1H-indol-3-yl) methyl) -3-methylimidazolidine-2,4-dione); 7-Cl-O-Nec-1

Peptide sequence: No

Appearance: Solid yellow

CAS #: 852391-15-2

Molecular formula: C₁₃H₁₂ClN₃O₂

Molecular weight: 277.71

Purity: ≥96% by TLC and LC-MS

Solubility: DMSO


CN1C (= O) C (NC1 = O) CC2 = CNC3 = C2C = CC = C3Cl


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)

InChi key


PubChem CID: 643953

Handling: Protect from light and moisture.

Storage conditions: -20 ° C

Shipping conditions: Gel Pack

USE: For research use only! It is not for use in humans.


Necrostatin-1 (NEC-1) is widely used in disease models to examine the contribution of receptor-interacting protein kinase (RIPK) 1 in cell death and inflammation. We studied three Nec-1 analogues: Nec-1, the active inhibitor of RIPK1, inactive Nec-1 (Nec-1i), its inactive variant, and stable Nec-1 (Nec-1s), its most stable variant. We report that Nec-1 is identical to methyl-thiohydantoin-tryptophan, an inhibitor of the potent immunomodulatory enzyme indolamine 2,3-dioxygenase (IDO).

Both Nec-1 and Nec-1i inhibited human IDO, but Nec-1 did not, as predicted by molecular modelling. Therefore, Nec-1s is a more specific RIPK1 inhibitor that lacks the targeting effect of IDO. Next, although Nec-1i was approximately 100 times less effective than Nec-1 in inhibiting human RIPK1 kinase activity in vitro, it was only 10 times less potent than Nec-1 and Nec-1s in a necroptosis assay. in mice and became even equipotent at high concentrations.

Along the same lines, in vivo, high doses of Nec-1, Nec-1i and Nec-1s equally well-prevented tumour necrosis factor (TNF) -induced mortality, excluding the use of NEC-1i as an inactive control. Paradoxically, low doses of Nec-1 or Nec-1i, but not Nec-1s, even sensitized mice to TNF-induced mortality. Importantly, Nec-1s did not show this low dose toxicity, again emphasizing the preferred use of Nec-1 in vivo. Our findings have important implications for the interpretation of Nec-1-based data in experimental disease models.

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