Necrostatin-7 (Nec-7) is a Necroptosis inhibitor with an EC₅₀ of 10.6 μM. Necrostatin-7 inhibits signal transduction from RANK to NFATc1 without affecting the activation of MAPK or NF-κB. Necrostatin-7 suppresses the expression levels of Acp5, Atp6v0d2, Ctsk and Dcstamp. Necrostatin-7 reduces myocardial infarction size, ameliorates adverse left ventricular remodeling, decreases myocardial wall stress, reduces the amount and length of scar tissue, and improves left ventricular function. Necrostatin-7 exerts cardioprotective effects in a rat model of permanent coronary artery occlusion. Necrostatin-7 can be used in research related to osteolytic bone diseases and myocardial infarction^[1][2][3][4].

Necrostatin-7 (0.1-3 μM; 3 days) dose-dependently inhibits M-CSF- and RANKL-induced osteoclast differentiation in primary bone marrow-derived macrophages at concentrations from 0.1 to 3 μM, with near-complete inhibition at 2 μM and 3 μM, without reducing BMM viability^[1].
Necrostatin-7 (1-3 μM; 5 days) dose-dependently inhibits osteoclastic bone resorption by primary bone marrow-derived macrophages at concentrations from 1 to 3 μM, with near-complete inhibition at 2 μM and 3 μM after 5 days of treatment^[1].
Necrostatin-7 (1-3 μM; 1-3 days) dose-dependently suppresses RANKL-induced expression of osteoclastogenic marker genes (Acp5, Atp6v0d2, Ctsk, Dcstamp) in primary bone marrow-derived macrophages at 1 μM and 3 μM over 1 to 3 days of differentiation^[1].
Necrostatin-7 (1-3 μM; 1-3 days) dose-dependently inhibits RANKL-induced NFATc1 autoamplification in primary bone marrow-derived macrophages at 1 μM and 3 μM over 1 to 3 days of differentiation, with near-complete suppression at 3 μM^[1].
Necrostatin-7 inhibits TNF-α-induced necroptosis in FADD-deficient human Jurkat T cells with an EC₅₀ of 10.6 μM^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Necrostatin-7 (14.5 mg/kg; i.p.; single dose 1 hour prior to permanent coronary occlusion) exerts cardioprotective properties, reducing myocardial wall stress (evidenced by lower NT-proBNP levels) and myocardial remodeling (evidenced by 9.0% infarct size) in rats with permanent coronary occlusion-induced myocardial infarction^[3].
Pretreatment with necrostatin-7 (14.5 mg/kg; i.p.) reduces left ventricular scar tissue and scar length, and lowers plasma N-terminal pro-brain natriuretic peptide levels, indicating improved left ventricular function in rats with permanent coronary occlusion-induced myocardial infarction^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

371.41

C₁₆H₁₀FN₅OS₂

351062-08-3

Solid

Light yellow to brown

O=C1N(C2=NC=CS2)C(S/C1=C\C3=CNN=C3C4=CC=C(F)C=C4)=N

Room temperature in continental US; may vary elsewhere.

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Fuji H, et al. Necrostatin-7 suppresses RANK-NFATc1 signaling and attenuates macrophage to osteoclast differentiation. Biochemical and biophysical research communications. 2018 Sep 05;503(2):544-549.  [Content Brief]

  [2]. Zheng W, et al. Structure-activity relationship study of a novel necroptosis inhibitor, necrostatin-7. Bioorganic & medicinal chemistry letters. 2008 Sep 15;18(18):4932-5.  [Content Brief]

  [3]. Dmitriev Y, et al. Necrostatin 7 Limits Myocardial Infarct Size and Reduces Cardiac Remodeling After Permanent Coronary Occlusion in Rats[J]. Circulation, 2014, 130(suppl_2): A17348-A17348.

  [4]. Dmitriev Y V, et al. CARDIOPROTFETIVE EFECTS OF NECROSTATIN-7 IN THE RAT MODEL OF PERMANENT CORONARY OCCLUSION[J]. Rossiiskii Fiziologicheskii Zhurnal Imeni IM Sechenova, 2015, 101(4): 408-414.