| Bioactivity | PNRI-299 is a selective AP-1 transcription inhibitor with an IC50 of 20 uM. PNRI-299 is a selective APE/Ref-1 inhibitor. PNRI-299 has no effect on NF-κB transcription or thioredoxin (up to 200 uM). PNRI-299 significantly reduces airway eosinophil infiltration, mucus hypersecretion, edema, and IL-4 levels in a mouse asthma model[1][2][3]. |
| Invitro | PNRI-299 specifically reacts with Ref-1, inhibits AP-1 transcription, and overexpression of the molecular target. Ref-1 attenuates PNRI-299 inhibition of AP-1 transcription. PNRI-299 interacts with the redox nucleophile Cys-65, to aid in the interpretation of structure activity relationships (SARs)[1]. |
| In Vivo | PNRI-299 (intranasal; 0.75 or 2.0 mg/kg; 30 min before OVA on days 25-27) reduces the airway inflammatory cell infiltration (arrows) and mucus release in ovalbumin (OVA)-treated (i.p.; 100 μg) female BALB/c mice aged 6-8 wk)[1]. PNRI-299 (3, 10 mg/kg; iv; 5 min before reperfusion) has no significant effect on the translocation of NF-κB in male C57/BL6 mice (8-10 weeks). PNRI-299 has little effect on the inflammatory response that follows intestinal I/R injury[2]. |
| Name | PNRI-299 |
| CAS | 550368-41-7 |
| Formula | C21H15N5O4 |
| Molar Mass | 401.37 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Reference | [1]. Nguyen C, et al. Chemogenomic identification of Ref-1/AP-1 as a therapeutic target for asthma. Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1169-73. [2]. Souza DG, et al. NF-kappaB plays a major role during the systemic and local acute inflammatory response following intestinal reperfusion injury. Br J Pharmacol. 2005 May;145(2):246-54. [3]. Sun Yang, et al. Apurinic/apyrimidinic endonuclease/redox effector factor-1(APE/Ref-1): a unique target for the prevention and treatment of human melanoma. Antioxid Redox Signal. 2009 Mar;11(3):639-50. |