| Field | Specification |
|---|---|
| Alternative names | Nec-1 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C13H13N3OS |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Necrostatin-1, also known as Nec-1, is a potent necroptosis inhibitor that crosses the blood-brain barrier, with an EC50 of 490 nM in Jurkat cells. It inhibits RIP1 kinase (EC50 182 nM) and also acts as an IDO inhibitor[1]. It is supplied as a light yellow to yellow solid (C13H13N3OS, MW 259.33) at 99.89% purity.
Physical & Chemical Properties
| CAS Number | 4311-88-0 |
|---|---|
| Molecular Formula | C13H13N3OS |
| Molecular Weight | 259.33 g/mol |
| Purity | 99.89% |
| Appearance | Solid |
| Color | Light yellow to yellow |
| SMILES | O=C(C(CC1=CNC2=C1C=CC=C2)N3)N(C)C3=S |
| Signaling Pathway | Apoptosis; Autophagy; Metabolic Enzyme/Protease |
| Solubility | In Vitro: DMSO: 100 mg/mL (385.61 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 1 year; -20°C, 6 months. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
Activity & Target
EC50: 182 nM (RIP1 kinase)[1]
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 100 mg/mL (385.61 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 1 year) or -20°C (up to 6 months); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.08 mg/mL (8.02 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (20.8 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.08 mg/mL (8.02 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (20.8 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% (50% EtOH + 50% Cremophor EL) + 90% saline |
|---|---|
| Result | 1.67 mg/mL (6.44 mM); suspension; requires sonication |
Direct preparation of the working solution
These formulations are prepared directly, without a DMSO stock; use them promptly after preparation.
Protocol 4
| Composition | 0.5% CMC-Na/saline water |
|---|---|
| Result | 12.5 mg/mL (48.20 mM); suspension; requires sonication |
Data provided by the manufacturer.
In Vitro
Necrostatin-1 (Nec-1) effectively blocks TNFα-induced necrotic death in L929 cells without the need for exogenous caspase inhibitors[1]. In the setting of radiocontrast media (RCM), Necrostatin-1 (Nec-1) prevents dilation of peritubular capillaries, pointing to a novel, cell death-independent role of the RIP1 kinase domain in regulating microvascular hemodynamics and in the pathophysiology of contrast-induced AKI (CIAKI)[2]. At 30 μM, Necrostatin-1 (Nec-1) raises the survival of cardiomyocyte progenitor cell (CMPCs) through inhibition of necrotic cell death[4].
In Vivo
Necrostatin-1 (Nec-1) causes tubular bilation and alters the kinetics of peritubular capillary dilation following RCM application. When a single intraperitoneal dose of Necrostatin-1 (1.65 mg/kg body weight, i.p.) is given 15 minutes before RCM, return to baseline levels is prevented during the observation period[2].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Cell Assay[3]
Seed C6 (3×105 cells/well) and U87 (1.5×105 cells/well) glioma cells onto a 96-well microplate and culture for 24 h. Add PBS to the control group and Shikonin to the experimental group to reach the final concentration. Assess cell viability by MTT assay after Shikonin treatment at the indicated time point, and read the absorbance value (A) at 570 nm on an automatic multi-well spectrophotometer. Treat two groups of glioma cells from the same cell line with Shikonin at a lower or higher concentration, respectively; treat two other groups for 1 h with 100 μM Necrostatin-1 or 40 μM z-VAD-fmk before co-incubation with Shikonin at the indicated concentration. In addition, treat another two groups of glioma cells with only 100 μM Necrostatin-1 or 40 μM Z-VAD-fmk at the corresponding time point[3].
Animal Administration
Mice[2] Use 8-10 week old male C57BL/6 mice (average weight approx.23 g). Administer 200 μL PBS or radiocontrast media (RCM) intravenously via the tail vein. 15 min. before RCM injection, give Z-VAD-fmk (10 mg/kg body weight) or Necrostatin-1 (1.65 mg/kg body weight) as a single intraperitoneal dose. Harvest mice another 24 hours after RCM application (48 hours after reperfusion). Collect blood samples by retroorbital bleeding and determine serum levels of urea and creatinine.
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Ferroptosis modulation enhances astrocyte-to-neuron conversion induced by a novel chemical cocktail in the hemorrhagic brain. Signal Transduct Target Ther 2026 Jul 29;11(1):309. PMID: 42527413
Disruption of heme homeostasis by nuclear receptor Nur77 induces pyroptosis through granzyme B-dependent GSDMC cleavage. Signal Transduct Target Ther 2025 Dec 17;10(1):413. PMID: 41407678
Erianin, a novel dibenzyl compound in Dendrobium extract, inhibits lung cancer cell growth and migration via calcium/calmodulin-dependent ferroptosis. Signal Transduct Target Ther 2020 May 8;5(1):51.
Interleukin-1α release during necrotic-like cell death generates myeloid-driven immunosuppression that restricts anti-tumor immunity. Cancer Cell 2024 Dec 9;42(12):2015-2031.e11. PMID: 39577420
Targeting TBK1 to overcome resistance to cancer immunotherapy. Nature 2023 Mar;615(7950):158-167. PMID: 36634707
Gut stem cell necroptosis by genome instability triggers bowel inflammation. Nature 2020 Apr;580(7803):386-390.
Stabilizing MARCH7 as a ferro-guardian against ferroptosis. Cell 2026 Jun 11;189(12):3553-3570.e30. PMID: 42049018
Red blood cells undergo lytic programmed cell death involving NLRP3. Cell 2025 May 29;188(11):3013-3029.e19. PMID: 40252640
Type III interferons induce pyroptosis in gut epithelial cells and impair mucosal repair. Cell 2024 Dec 26;187(26):7533-7550.e23. PMID: 39500322
Therapeutic application of human type 2 innate lymphoid cells via induction of granzyme B-mediated tumor cell death. Cell 2024 Feb 1;187(3):624-641.e23. PMID: 38211590
