ALT-007 is an orally active serine palmitoyltransferase ( SPT ) inhibitor that selectively reduces the levels of toxic very-long-chain deoxysphingolipids to enhance protein homeostasis. ALT-007 restores aging-related loss of muscle mass in a mouse model of sarcopenia. ALT-007 enhances protein homeostasis in both mouse and C. elegans models of aging and disease. ALT-007 can be used for age-related neuromuscular diseases research [1].
In Vivo, ALT-007 (1 mg/kg, p.o. (mixed with the food), daily for 20 weeks) enhances physical fitness in aged mice model of sarcopenia, evidenced by improved muscle function and aerobic capacity[1]. ALT-007 (1 and 5 μM) ameliorates age-related decline across species, improving proteostasis to extend lifespan and reduce proteotoxicity in C. elegans[1]. ALT-007 (4 mg/kg, p.o. (mixed with the food), daily for 10 days) is well-tolerated and effectively reduces muscle ceramide levels in mice[1].
In Vitro, ALT-007 (10 nM-10 μM) reduces ceramide levels in immortalized mouse C2C12 myoblasts at 10 nM, comparable to Myriocin [1].
References:
[1]. Poisson J, et al. Safe and Orally Bioavailable Inhibitor of Serine Palmitoyltransferase Improves Age-Related Sarcopenia. ACS Pharmacol Transl Sci. 2024 Dec 29;8(1):203-215.
In Vivo, ALT-007 (1 mg/kg, p.o. (mixed with the food), daily for 20 weeks) enhances physical fitness in aged mice model of sarcopenia, evidenced by improved muscle function and aerobic capacity[1]. ALT-007 (1 and 5 μM) ameliorates age-related decline across species, improving proteostasis to extend lifespan and reduce proteotoxicity in C. elegans[1]. ALT-007 (4 mg/kg, p.o. (mixed with the food), daily for 10 days) is well-tolerated and effectively reduces muscle ceramide levels in mice[1].
In Vitro, ALT-007 (10 nM-10 μM) reduces ceramide levels in immortalized mouse C2C12 myoblasts at 10 nM, comparable to Myriocin [1].
References:
[1]. Poisson J, et al. Safe and Orally Bioavailable Inhibitor of Serine Palmitoyltransferase Improves Age-Related Sarcopenia. ACS Pharmacol Transl Sci. 2024 Dec 29;8(1):203-215.