Calcipotriene

Calcipotriol inhibited the growth of SCC13 cells as determined by MTT assay and PCNA staining, and stimulated cell differentiation as confirmed by involucrin immunocytochemical staining, but did not induce apoptosis as shown by DAPI staining. Western blot analysis demonstrated that calcipotriol specifically dephosphorylated 170- and 66-kDa polypeptides from 8 hours post-treatment, with complete dephosphorylation observed at 12 hours. These polypeptides were confirmed as epidermal growth factor receptor and Shc, respectively. Calcipotriol-mediated EGF receptor dephosphorylation required the presence of extracellular calcium, and similar kinetics of dephosphorylation were observed in HaCaT cells cultured in high calcium concentration medium. BrdU labeling confirmed the calcium dependency of calcipotriol for inhibition of cell proliferation.
EGF receptor deactivation by calcipotriol represents a possible mechanism of action for the inhibition of cell proliferation and the stimulation of differentiation in SCC13 cells and HaCaT cells.

Fig. 1 Effect of calcipotriol (Calcipotriene) on cell growth, proliferation, apoptosis, and differentiation of SCC13 cells. (Lee E A.; et al. 2001)

A ROS-sensitive nano-micelle percutaneous delivery system encapsulating calcipotriene was developed using methoxypolyethylene glycol-thioether-thiol as the carrier material. The nano-micelles exhibited ROS-responsive drug release triggered by the psoriatic skin microenvironment. In vivo studies using imiquimod-induced psoriasis-like mouse models demonstrated that the nano-micelles effectively ameliorated psoriatic inflammation. The ROS-sensitive release mechanism enhanced drug accumulation at the target site, improving therapeutic efficacy compared to conventional calcipotriene formulations.

Fig. 2 Preparation and characterization of mPEG-SS-calcipotriol. (Hua Y.; et al. 2022)