ChemicalBook CAS DataBase List 1120332-55-9

1120332-55-9

Name	1H-Indol-7-amine, 5-[(1,1-dioxido-4-thiomorpholinyl)methyl]-2-phenyl-N-(tetrahydro-2H-pyran-4-yl)-
CAS	1120332-55-9
Molecular Formula	C24H29N3O3S
Molecular Weight	439.57
MOL File	1120332-55-9.mol

Chemical Properties

Boiling point	736.2±60.0 °C(Predicted)
density	1.319±0.06 g/cm3(Predicted)
solubility	Acetonitrile: Slightly soluble: 0.1-1 mg/ml DMSO: Sparingly soluble: 1-10 mg/ml
form	Solid
pka	17.48±0.30(Predicted)
color	Off-white to yellow
Cosmetics Ingredients Functions	ANTIOXIDANT SKIN PROTECTING

Hazard Information

Uses

NecroX-7 is a potent free radical scavenger and a HMGB1 (high-mobility group box 1) inhibitor. NecroX-7 can be used as an antidote to acetaminophen toxicity. NecroX-7 exerts a protective effect by preventing the release of HMGB1 in ischemia/reperfusion injury. NecroX-7 inhibits the HMGB1-induced release of TNF and IL-6, as well as the expression of TLR-4 and receptor for advanced glycation end products. NecroX-7 can be used graft-versus-host disease (GVHD) research[1].

in vivo

NecroX-7 (0-0.3 mg/kg, IV, once injection at 2-d intervals, for 2 weeks) significantly attenuates GVHD-related mortality and inhibits severe tissue damage^[1].
NecroX-7 protects mice against lethal GVHD by reciprocal regulation of regulatory T/Th1 cells, attenuating systemic HMGB1 accumulation and inhibiting HMGB1-mediated inflammatory response^[1].

Animal Model:	Female BALB/c and C57BL/6 mice (Eight-week-old, with GVHD)^[1]
Dosage:	0.03, 0.1, and 0.3 mg/kg
Administration:	IV, once injection at 2-d intervals, for 2 weeks
Result:	Observed statistically significant prolonged survival at doses ≥0.1 mg/kg: 30–60% of mice in these treatment groups survived for >50 d. Significantly improved clinical signs and prolonged survival, and the mice showed a reduction in clinical manifestations of acute GVHD, including weight loss, hunched posture, diarrhea, and ruffled fur.

IC 50

IL-6; TLR4

References

[1] Im KI, et al. The Free Radical Scavenger NecroX-7 Attenuates Acute Graft-versus-Host Disease via Reciprocal Regulation of Th1/Regulatory T Cells and Inhibition of HMGB1 Release. J Immunol. 2015 Jun 1;194(11):5223-32. DOI:10.4049/jimmunol.1402609

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