|Program/MOA||Therapeutic Area||IND-Enabling||Phase 1||Phase 2||Phase 3|
|LP3525-HT2c Superagonist||DEEs and other refractory epilepsies|
|LP143CB2 Agonist||ALS and other neuroinflammatory disorders|
|LP659S1P Receptor Modulator||Multiple neuroinflammatory disorders|
|Program||Area||Stage||LP3525-HT2c Superagonist||DEEs and other refractory epilepsies||Phase 1|
|LP143CB2 Agonist||ALS and other neuroinflammatory disorders||IND-Enabling|
|LP659S1P Receptor Modulator||Multiple neuroinflammatory disorders||IND-Enabling|
*Additional earlier discovery stage compounds in development
LP352 is an oral, centrally acting, 5-HT2c superagonist in development for the potential treatment of DEEs such as Dravet syndrome and Lennox-Gastaut syndrome (LGS) and other epileptic disorders. LP352 is designed to modulate GABA inhibition and, as a result, suppress the hyperexcitability that is characteristic of seizures. LP352 has demonstrated negligible observed impact on 5-HT2b and 5-HT2a receptor subtypes in our preclinical studies to date. 5-HT2b and 5-HT2a receptor agonism have been associated with significant adverse side effects. LP352 has novel chemistry and attributes, and was designed to be more specific and selective for the 5-HT2c receptor subtype, giving it the potential to reduce seizures in DEE patients while overcoming the known or perceived safety limitations of available drugs in the 5-HT2 class.
LP143 is a centrally acting, full CB2 agonist in development for neurodegenerative diseases associated with neuroinflammation, including amyotrophic lateral sclerosis (ALS). CB2 agonism has been shown in preclinical studies to regulate neuroinflammatory processes, reducing the neuronal damage characteristic of degeneration. We believe there is a strong rationale for CB2 agonism in a range of neurodegenerative diseases, given increased CB2 expression in patients with these diseases as well as results from animal models. LP143, through its selectivity for CB2 versus the cannabinoid type 1 receptor (CB1), was designed to minimize the risk of psychoactive adverse events associated with CB1 activation. In preclinical studies, LP143 has demonstrated 1,000-fold greater selectivity for CB2 over CB1, sustained activity over the duration of treatment, and favorable blood-brain-barrier penetration.
LP659 is a centrally acting, S1P receptor subtypes 1 and 5 (S1P1,5) modulator for which aberrant modulation has been shown to be involved in a wide range of neurodegenerative diseases, including multiple sclerosis, lupus, Parkinson’s disease and Alzheimer’s disease. We believe LP659’s potential selectivity and specificity could result in a superior profile in the clinic compared to drugs that may not fully engage the intended GPCR target, may cause off-target activity, or may be associated with other undesirable effects.
*LP352, LP143 and LP659 are investigational compounds that are not approved by regulatory authorities for commercial sale in any country.