Key result
In PAH rat models, CAR-modified liposomes of SOD plus fasudil given every 72 hours produced a >50% reduction in mPAP and was as efficacious as plain drugs given every 48 hours.
Why the study?
Does a CAR-modified liposomal formulation of SOD and fasudil improve pulmonary hemodynamics and slow disease progression in rat models of PAH compared to plain drugs?
Does a CAR-modified liposomal formulation of SOD and fasudil improve pulmonary hemodynamics and slow disease progression in rat models of PAH compared to plain drugs?
A targeted liposomal formulation of SOD and fasudil reduces pulmonary arterial pressure and slows PAH progression in rat models at a reduced dosing frequency compared to plain drugs.
Remains preclinical and should not change practice; leaves open human translation of CAR-modified liposomes for PAH.
Currently, two or more pulmonary vasodilators are used to treat pulmonary arterial hypertension (PAH), but conventional vasodilators alone cannot reverse disease progression. In this study, we tested the hypothesis that a combination therapy comprising a vasodilator plus a therapeutic agent that slows pulmonary arterial remodeling and right heart hypertrophy is an efficacious alternative to current vasodilator-based PAH therapy. Thus, we encapsulated a cocktail of superoxide dismutase (SOD), a superoxide scavenger, and fasudil, a specific rho-kinase inhibitor, into a liposomal formulation equipped with a homing peptide, CAR. We evaluated the effect of the formulations on pulmonary hemodynamics in monocrotaline-induced PAH rats (MCT-induced PAH) and assessed the formulation's efficacy in slowing the disease progression in Sugen-5416/hypoxia-induced PAH rats (SU/hypoxia-induced PAH). For acute studies, we monitored both mean pulmonary and systemic arterial pressures (mPAP and mSAP) for 2 to 6 h after a single dose of the plain drugs or formulations. In chronic studies, PAH rats received plain drugs every 48 h and the formulations every 72 h for 21 days. In MCT-induced PAH rats, CAR-modified liposomes containing fasudil plus SOD elicited a more pronounced, prolonged, and selective reduction in mPAP than unmodified liposomes and plain drugs did. In SU/hypoxia-induced PAH rats, the formulation produced a >50% reduction in mPAP and slowed right ventricular hypertrophy. When compared with individual plain drugs or combination, CAR-modified-liposomes containing both drugs reduced the extent of collagen deposition, muscularization of arteries, increased SOD levels in the lungs, and decreased the expression of pSTAT-3 and p-MYPT1. Overall, CAR-modified-liposomes of SOD plus fasudil, given every 72 h, was as efficacious as plain drugs, given every 48 h, suggesting that the formulation can reduce the total drug intake, systemic exposures, and dosing frequency.
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Gupta et al. (2017) studied Pulmonary arterial hypertension (PAH). CAR-modified liposomes containing fasudil plus superoxide dismutase (SOD) vs. plain drugs given every 48 h was evaluated on mean pulmonary arterial pressure (mPAP). In PAH rat models, CAR-modified liposomes of SOD plus fasudil given every 72 hours produced a >50% reduction in mPAP and was as efficacious as plain drugs given every 48 hours.
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