The 11-hydroxy metabolites of Delta(8).- and Delta(9)-tetrahydrocannabinol are more active than the parent compounds when administered to mice by either the intravenous or intracerebral route. Both Delta(8)- and Delta(9)-tetrahydrocannabinol are rapidly and extensively metabolized by the liver and not by the brain. The hypothesis that the 11-hydroxy metabolites may be the active form of tetrahydrocannabinol is discussed

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Cranial retardation was produced in the offspring of CF1 mice that were treated with norethynodrel [17α‐ethynyl‐estr‐5(10)‐en‐3‐on‐17β‐ol] or its metabolites [17α‐ethynyl‐estr‐5(10)‐ene‐3α,17β‐diol and the corresponding 3β,17β‐diol] on days 8–10 of gestation. The most active agent was the 3β,17β‐diol. Incomplete development of the parietal bones was observed in 64.1% of fetuses examined from mothers treated with 0.6 mg/kg of the 3β,17β‐diol. Five percent of all fetuses in this treatment group had exencephaly. An anomaly resembling cryptorchidism occurred when the diols were administered on gestation days 11–13.