CD 437 is a selective agonist of RARγ [1].

Retinoic acid receptor gamma (RAR-γ) is a nuclear receptor that is activated by 9-cis retinoic acid and all-trans retinoic acid. RAR-γ also functions as a transcription factor.

CD 437 is a selective RARγ agonist. In tumor cells, CD437 induced RAR-γ-dependent differentiation and apoptosis. Also, CD437 induced DNA adduct formation and p53-independent DNA damage response [1]. In DU145 human prostate cancer cells, CD437 rapidly reduced IκBα and increased nuclear translocation of the NF-κB subunit p65. Also, CD437 increased the DNA-binding activity of NF-κB and induced DR4 expression and apoptosis [2]. In human melanoma A375 cells, CD437 induced apoptosis, which was mediated by the activation of NF-κB and RIG-I (retinoic acid inducible gene I) pathway [3]. In human osteosarcoma cells, CD437 activated c-Jun N-terminal kinase 1 (JNK1) through the upregulation of thioredoxin-binding protein 2 (TBP2) and induced apoptosis. Also, CD437 induced TBP2 mRNA expression by recruitment of ETS1 transcription factor [4].

References:
[1].  Zhao X, Spanjaard RA. The apoptotic action of the retinoid CD437/AHPN: diverse effects, common basis. J Biomed Sci, 2003, 10(1): 44-49.
[2].  Jin F, Liu X, Zhou Z, et al. Activation of nuclear factor-kappaB contributes to induction of death receptors and apoptosis by the synthetic retinoid CD437 in DU145 human prostate cancer cells. Cancer Res, 2005, 65(14): 6354-6363.
[3].  Pan M, Geng S, Xiao S, et al. Apoptosis induced by synthetic retinoic acid CD437 on human melanoma A375 cells involves RIG-I pathway. Arch Dermatol Res, 2009, 301(1): 15-20.
[4].  Hashiguchi K, Tsuchiya H, Tomita A, et al. Involvement of ETS1 in thioredoxin-binding protein 2 transcription induced by a synthetic retinoid CD437 in human osteosarcoma cells. Biochem Biophys Res Commun, 2010, 391(1): 621-626.