SP-C Inhibitors

The class of compounds known as SP-C inhibitors includes various chemicals that either directly or indirectly modulate the function of surfactant protein C (SP-C), a critical component of pulmonary surfactant. Amiodarone and chloroquine indirectly impact SP-C through lysosomal dysfunction, disrupting SP-C processing and maturation. Brefeldin A directly inhibits SP-C trafficking by disrupting Golgi apparatus function, compromising the incorporation of SP-C into surfactant. Nelfinavir induces ER stress, influencing SP-C through misfolding and degradation.

Azithromycin, bafilomycin A1, and tunicamycin affect SP-C indirectly by targeting mitochondrial function, lysosomal acidification, and N-linked glycosylation, respectively. Dexamethasone modulates SP-C transcriptionally by interacting with glucocorticoid receptors. Rapamycin, an mTOR inhibitor, influences cellular processes related to surfactant synthesis, impacting SP-C production. Concanamycin A disrupts lysosomal acidification, affecting SP-C processing, and degradation. Ketoconazole, an antifungal agent, influences SP-C by impacting cholesterol homeostasis. 4-Phenylbutyrate, acting as a chemical chaperone, mitigates ER stress, promoting proper folding and trafficking of SP-C.