crRASP

Scientific evidence

• RASP, administered orally at 50 mg/Kg to rats over two generations, showed no adverse effects on growth, characteristics, reflexes, or organ health[1].
• In a comparative in vivo study, RASP showed four times more potent anti-inflammatory effects on rat paw oedema compared to tretinoin[2].
• In an in vitro study, it was observed that RASP exhibited potent inhibitory effects on lipoxygenase, the crucial components of a biochemical pathway with a significant involvement in inflammation and immune response[2].
• RASP significantly inhibits the production of IL-2 and IFN-γ by CD4+ and CD8+ cells, in contrast to the presently available retinoids, including tretinoin, and their isomers or esters. This suggests that RASP may have potential as an immunosuppressant drug[3].
• Both tretinoin and RASP dose-dependently inhibited angiogenesis in the chicken embryo chorioallantoic membrane model, but RASP was more effective and could be used in a wider dose range due to lower toxicity compared with Tretinoin[4].
• Both tretinoin and RASP decreased the number of HUVEC and prostate cancer cells in a dose-dependent manner. RASP was less cytotoxic than tretinoin on HUVEC cells, but more effective and potent on prostate cancer cells[4].
• RASP inhibits RNase P, a key enzyme in protein synthesis at lower concentrations than retinoids. This suggests that RASP may be a more effective treatment for skin conditions that require increased protein synthesis such as psoriasis[5].
• RASP has been shown to be effective against cancer. It works by regulating the expression of genes and miRNAs that are involved in apoptosis and the cell cycle[6].