3-Aminobenzamide - CAS 3544-24-9
Not Intended for Therapeutic Use. For research use only.
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3-Aminobenzamide is a competitive PARP inhibitor with Ki of 1.8 μM.
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CAS 3544-24-9 3-Aminobenzamide

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Reference Reading

1.Phase I study of iniparib concurrent with monthly or continuous temozolomide dosing schedules in patients with newly diagnosed malignant gliomas.
Blakeley JO1, Grossman SA2, Mikkelsen T3, Rosenfeld MR4, Peereboom D5, Nabors LB6, Chi AS7, Emmons G8, Garcia Ribas I8, Supko JG7, Desideri S2, Ye X2. J Neurooncol. 2015 Oct;125(1):123-31. doi: 10.1007/s11060-015-1876-0. Epub 2015 Aug 19.
Iniparib is a prodrug that converts to highly reactive cytotoxic metabolites intracellularly with activity in preclinical glioma models. We investigated the maximum tolerated dose (MTD) of iniparib with monthly (m) and continuous (c) temozolomide (TMZ) dosing schedules in patients with malignant gliomas (MG). Adults with newly diagnosed MG who had successfully completed ≥80% of radiation (RT) and TMZ without toxicity received mTMZ dosing (150-200 mg/m(2) days 1-5/28 days) or cTMZ dosing (75 mg/m(2)/days × 6 weeks) in conjunction with iniparib (i.v. 2 days/week) in the adjuvant setting. Iniparib was dose escalated using a modified continual reassessment method (mCRM). 43 patients (32 male; 34 GBM, 8 AA, 1 gliosarcoma; median age 54 years; median KPS 90) were enrolled across 4 dose levels. In the mTMZ group, 2/4 patients had dose limiting toxicities (DLT) at 19 mg/kg/week (rash/hypersensitivity). At 17.2 mg/kg/week, 1/9 patients had a DLT (grade 3 fatigue).
2.Poly(ADP-ribosyl)ation is involved in pro-survival autophagy in porcine blastocysts.
Lee HR1, Gupta MK2, Kim DH1, Hwang JH1, Kwon B1, Lee HT1. Mol Reprod Dev. 2016 Jan;83(1):37-49. doi: 10.1002/mrd.22588. Epub 2015 Oct 19.
Poly(ADP-ribosyl)ation (PARylation) prevents apoptosis through its involvement in pro-survival autophagy in cultured cells; whether or not the same is true for pre-implantation embryos has not yet been documented. In this study, we investigated the participation of PARylation and autophagy in in vitro porcine pre-implantation embryo development. The transcript levels of autophagy-related genes and poly(ADP-ribose) polymerase 1 (PARP1), an enzyme required for PARylation, were transiently up-regulated by fertilization, decreased at the late 1-cell stage, and maintained until the blastocyst stage. LC3, a marker of autophagosomes, and poly(ADP-ribose) (PAR) polymer were present in all stages of pre-implantation development. Exposure of embryos to 3-methyladenine, an autophagy inhibitor, or 3-aminobenzamide, a PARP inhibitor, suppressed the development of blastocysts. Pharmacological inhibition of PARylation further suppressed pro-survival autophagy by decreasing the expression of autophagy-related genes (ATG5, BECLIN1, and LC3) and decreasing LC3 protein abundance while increasing the rate of apoptosis in blastocysts.
3.PARP inhibition attenuates neuroinflammation and oxidative stress in chronic constriction injury induced peripheral neuropathy.
Komirishetty P1, Areti A1, Yerra VG1, Pk R2, Sharma SS2, Gogoi R3, Sistla R4, Kumar A5. Life Sci. 2016 Apr 1;150:50-60. doi: 10.1016/j.lfs.2016.02.085. Epub 2016 Feb 24.
AIM: Peripheral nerve degeneration after nerve injury is accompanied with oxidative stress that may activate poly ADP-ribose polymerase (PARP, DNA repair enzyme). PARP overactivation amplifies the neuronal damage either due to energy crisis or through inflammatory process by facilitating nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). Hence investigated the role of PARP inhibitors, 3-Aminobenzamide (3-AB) and 1,5-isoquinolinediol (ISO) in the attenuation of chronic constriction injury (CCI) induced peripheral neuropathy in rats.
4.Edaravone abrogates LPS-induced behavioral anomalies, neuroinflammation and PARP-1.
Sriram CS1, Jangra A1, Gurjar SS2, Mohan P3, Bezbaruah BK4. Physiol Behav. 2016 Feb 1;154:135-44. doi: 10.1016/j.physbeh.2015.10.029. Epub 2015 Oct 30.
Poly(ADP-ribose) polymerase-1 (PARP-1) is a DNA nick-sensor enzyme that functions at the center of cellular stress response and affects the immune system at several key points, and thus modulates inflammatory diseases. Our previous study demonstrated that lipopolysaccharide (LPS)-induced depressive-like behavior in mice can be ameliorated by 3-aminobenzamide, which is a PARP-1 inhibitor. In the present study we've examined the effect of a free radical scavenger, edaravone pretreatment against LPS-induced anxiety and depressive-like behavior as well as various hippocampal biochemical parameters including PARP-1. Male Swiss albino mice were treated with edaravone (3 & 10mg/kgi.p.) once daily for 14days. On the 14th day 30min after edaravone treatment mice were challenged with LPS (1mg/kgi.p.). After 3h and 24h of LPS administration we've tested mice for anxiety and depressive-like behaviors respectively. Western blotting analysis of PARP-1 in hippocampus was carried out after 12h of LPS administration.