Isolation from cannabis sativa L. of cannflavin—a novel inhibitor of prostaglandin production

1 H NMR and HPLC/DAD for Cannabis sativa L. chemotype distinction, extract profiling and specification

“…Enrichment without parallel concentration of cannabinoids (or other phenolics) may only be achieved with more sophisticated fractionation and chromatographic techniques. Despite some interesting biological activities when applied alone 8) , cannflavins may play no direct role in the activity of conventional extracts and serve as indicator for identity without need for specification.…”

“…Meanwhile other non-psychotropic, non-CB binding cannabinoids, mainly cannabidiol (CBD) [5,6] but also cannabigerol (CBG) [7], are increasingly investigated showing partly distinct effects. Moreover activities are reported for minor non-cannabinoid co-constituents such as the prenylated flavone cannflavin A [8] (CFL-A), common flavonoids [9] or terpenes [10,11]. Despite or because of the complexity some authors advocate the advantage of the natural mixtures with combinations of cannabis constituents [12,13] primarily determined by the chemovar.…”

Cannabinoids, Endocannabinoids, and Related Analogs in Inflammation

“…The values shown are the prostaglandin concentrations (pg/ml) divided by number of adherent cells the geranylated flavone cannflavin A (Fig. 5), is 30 times more potent than aspirin as an inhibitor of prostaglandin E 2 (114,115). These potentially important findings have been overlooked, as most attention in marijuana research has been directed to the analgesic effects of the plant and to mechanisms of psychoactivity.…”

The medicinal uses of cannabis and its constituents

“…However, Evans et al (1987a) reported that several cannabinoids including A'-THC exhibited a stimulation followed by inhibition of phospholipase A2 in cell-free assays and further demonstrated that a range of cannabinoidal constituents would inhibit both cyclo-oxygenase and lipoxygenase depending upon their concentration (Evans ef al., 1987b). This possibly explains the observation of Barrett et al (1985) that cannabinoids inhibited release of PGEz from human rheumatoid synovial cells. It is Iikely that the receptor to A'-THC or its metabolites is sensitive to or dependent upon PG levels but is not directly located in the cascade.…”