Dicyclomine Hydrochloride

Dicyclomine hydrochloride inhibited the in vitro growth and virulence factors of Candida albicans, including adhesion, early biofilm, mature biofilm, and planktonic growth. The drug effectively blocked the yeast-to-hyphal transition in various inducer media such as serum, proline, glucose, and N-acetylglucosamine, and could kill fungal cells within 15 minutes of exposure. The mechanism of action involved targeting signal transduction pathways, as demonstrated by RT-PCR analysis. Dicyclomine upregulated eight genes including Bcy1, Tup1, and Mig1, while downregulating Ume6, Ece1, and Pde2 genes involved in the cAMP signaling pathway, as well as the DNA binding protein gene Rfg1. The drug significantly upregulated the master negative regulator of hyphal formation, Tup1.

Fig. 1 Dicyclomine targets signal transduction pathways in C. albicans. (Ali A.; et al. 2018)

Hydroxypropylmethylcellulose-based microsponges loaded with dicyclomine hydrochloride were fabricated using a quasi-emulsion solvent diffusion method for colon-targeted delivery. The microsponges exhibited enhanced production yield, drug content, and encapsulation efficiency with increasing drug-polymer ratio, and demonstrated greater thermal stability compared to the pure drug. In vitro dissolution studies at pH 1.2, 6.8, and 7.4 showed that drug release decreased with higher polymer concentration. Pharmacokinetic evaluation in rabbits revealed increased t1/2, tmax, Cmax, and AUC0-t values for the microsponge formulation compared to standard dicyclomine, indicating enhanced bioavailability.