CB2-Selective Program: Cannabinor
It is only in the past decade that the scientific and medical communities have begun to understand the physiological importance of the two known cannabinoid receptors, CB1 and CB2, and their signaling pathways. Their impact on human health and disease is being studied in such diverse biological responses as pain, impulse control, inflammation and immunomodulation. In humans, CB1 receptors are found mainly in the central nervous system, and their activation leads to the psychotropic and cardiovascular effects of cannabis. CB2 receptors are found primarily in peripheral immune cells, and their activation have been shown to modulate inflammatory and immunoregulatory pathways.
Pharmos Corp focuses on identifying compounds from its synthetic cannabinoid library that preferentially activate the CB2 receptor relative to the CB1 receptor. For some indications it is becoming clear that a balanced activation of both CB1 and CB2 pathways may be optimal, while for other indications pure CB2 activity may be preferable. Cannabinor is the first lead candidate to emerge from this body of Pharmos’ proprietary technology.
Cannabinor (formerly referred to as PRS-211,375), a synthetic CB2-selective agonist, is in Phase 2 clinical testing as an analgesic. In January 2007, Pharmos reported that in a Phase 2a experimentally induced pain model, cannabinor failed to meet the primary endpoint of reducing capsaicin-induced pain. However, the Company subsequently noted that compared to placebo, i.v. cannabinor did exhibit a statistically significant systemic analgesic effect against pressure-induced and heat-induced pain. In April 2007, Pharmos reported that in a separate Phase 2a trial of i.v. cannabinor in acute nociceptive pain in patients undergoing 3rd molar dental extraction, an analgesic effect was observed at the 12mg dose; however, there was no effect at the higher doses (24mg and 48mg). This was an unexpected pattern of results and the Company decided to cease the development of IV cannabinor for pain indications and explore possible collaborations towards retargeting of cannabinor. In both Phase 2a trials, cannabinor was generally well tolerated with no serious adverse events.
Cannabinor has demonstrated efficacy in a number of preclinical animal models of pain, inflammation and autoimmune disease. Analgesic activity has been documented in nociceptive, neuropathic, visceral and inflammatory pain in rodents and in post-operative pain in a porcine surgery model. The magnitude of analgesia was generally equivalent or greater than that of accepted comparator agents, including morphine or non-steroidal anti-inflammatory drugs (NSAIDS). In a number of models where duration of analgesia was measured, cannabinor remained effective at reducing pain significantly longer than morphine. Preliminary evidence from preclinical studies also suggests that tolerance to the therapeutic effect of cannabinor might not occur. Tolerance to narcotics such as morphine, on the other hand, can be a large clinical problem, with patients requiring steadily increasing doses to maintain therapeutic effect. A drug that remains effective without increasing dosage would be a valuable advance in treating severe pain.
Characteristically, cannabinoid compounds are lipophilic, a property making it difficult to formulate these compounds for oral administration. Importantly, cannabinor is water-soluble, and in animal models where the drug was administered orally, significant efficacy was measured. Thus, preliminary evidence suggests that oral administration may be feasible as development proceeds. In addition to its analgesic effect, cannabinor’s immunomodulatory potential has been measured in animal models of multiple sclerosis (MS), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). In monophasic and relapsing models of MS, cannabinor performed as well or better than currently available treatments. In the complete Freund’s adjuvant (CFA)-induced RA model, cannabinor protected tissue from morphological damage and ameliorated pain. In the IBD model, cannabinor treatment resulted in normal weight gain and improved tissue morphology.