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ChemicalBook--->CAS DataBase List--->1093131-03-3

1093131-03-3

1093131-03-3 Structure

1093131-03-3 Structure
IdentificationBack Directory
[Name]

Veledimex (S enantiomer)
[CAS]

1093131-03-3
[Synonyms]

INXN-1001 S enantiome
RG-115932 S enantiome
Veledimex (S entiomer)
Veledimex (S enantiomer)
Benzoic acid, 2-ethyl-3-methoxy-, 2-(3,5-dimethylbenzoyl)-2-[(1S)-1-(1,1-dimethylethyl)butyl]hydrazide
[Molecular Formula]

C27H38N2O3
[MDL Number]

MFCD31382195
[MOL File]

1093131-03-3.mol
[Molecular Weight]

438.6
Chemical PropertiesBack Directory
[density ]

1.048±0.06 g/cm3(Predicted)
[storage temp. ]

Store at -20°C
[solubility ]

Soluble in DMSO
[form ]

Solid
[pka]

10.28±0.46(Predicted)
[color ]

Light yellow to yellow
Hazard InformationBack Directory
[Uses]

Veledimex S enantiomer (INXN-1001 S enantiomer) is the S enantiomer of veledimex. Veledimex is an oral activator ligand for a proprietary gene therapy promoter system, and a moderate inhibitor of and substrate for CYP3A4/5[1].
[in vivo]

Veledimex generally has moderate to low oral bioavailability after a single oral administration in mice and monkeys (-56% in mice and up to 17.4% in cynomolgus monkeys) with mostly low plasma clearance (1399 and 1170 mL/h per kilogram in mice and monkeys, respectively), high volume of distribution (20271 and 9180 mL/h per kilogram in mice and monkeys, respectively), and long terminal half-lives (-10 hours in mice and -30 hours in monkeys) after intravenous administration[1]. Ad-RTS-mIL-12 + veledimex have demonstrated a dose-related increase in tumor IL-12 mRNA and IL-12 protein expression. Discontinuation of veledimex resulted in a return to baseline IL-12 mRNA and protein expression in numerous syngeneic mouse tumor models. Veledimex crosses the blood-brain-barrier in both naive and orthotopic GL-261 mice with increased brain tissue level of -6 fold observed in tumor bearing vs. normal mice. Ad-RTS-mIL-12 + veledimex demonstrate a dose-related increase in survival without significant adverse events[2].

[IC 50]

IL-1
[References]

[1] Barrett JA, et al. Regulated intratumoral expression of IL-12 using a RheoSwitch Therapeutic System? (RTS?) gene switch as gene therapy for the treatment of glioma. Cancer Gene Ther. 2018;25(5-6):106-116. DOI:10.1038/s41417-018-0019-0
[2] John A. Barrett, INTRATUMORAL REGULATED EXPRESSION OF IL-12 AS A GENE THERAPY APPROACH TO TREATMENT OF GLIOMA. Neuro Oncol. 2015 Nov; 17(Suppl 5): v113.
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