CBN

The main cannabinoid receptor in the brain, responsible for THC’s intoxicating effects, binds CBN with a Ki of approximately 211 nM, compared with about 40.7 nM for Delta-9-THC, meaning Delta-9-THC shows roughly 5.2x stronger CB1 binding affinity.

CBN acts as a weak partial CB1 agonist. A human-receptor research found an EC50 of approximately 4 µM for CBN versus 0.4 µM for Delta-9-THC, making CBN roughly 10x less potent in that signalling pathway. Its maximum response was also substantially lower, around 29% versus 72% for THC. Human research further found that 50 mg oral CBN alone did not produce the characteristic intoxication caused by 25 mg THC.

Considering its approximately 5x weaker CB1 binding, 10x lower functional potency, much lower maximum receptor response and limited THC-like effects in humans, CBN is theoretically estimated at around 0.1x the psychoactive potency of Delta-9-THC. This is an evidence-based estimate rather than a directly measured human potency ratio.

The main cannabinoid receptor in the immune system, involved in regulating immune cell activity and inflammatory responses. CBN binds CB2 with a Ki of approximately 126 nM, compared with around 36.4 nM for Delta-9-THC, meaning Delta-9-THC shows approximately 3.5x stronger CB2 binding affinity.

CBN can act as a CB2 agonist, with an early functional assay reporting an EC50 of 261 nM. However, newer human-receptor experiments found negligible CB2 activation below 10 µM, showing that its functional activity varies substantially between experiments. CB2-mediated immune or inflammatory effects therefore remain plausible, but their importance in humans has not been established.

Voltage-gated sodium channels help sensory nerves generate electrical signals, including those involved in transmitting pain. CBN inhibits human NaV1.7 and NaV1.8, with NaV1.7 IC50 values of approximately 10.7 to 29.9 µM.

Inhibiting these channels can make pain-sensing nerves less likely to become activated and repeatedly transmit pain signals. This could potentially contribute to reduced pain sensitivity and less persistent pain signalling, although these effects have not been confirmed clinically in humans.

TRP channels help sensory nerves detect temperature, irritation and pain-related signals. CBN strongly activates TRPA1 with an EC50 of approximately 0.18 µM and blocks the cold-sensing TRPM8 channel with an IC50 of approximately 0.21 µM. CBN also activates TRPV2, TRPV3 and TRPV4, although generally only at higher concentrations.

Together, these interactions likely influence pain, temperature sensitivity and inflammatory responses, although their exact contribution to CBN’s effects in humans remains uncertain.

Human liver enzymes convert CBN into several metabolites, including 11-OH-CBN.

Animal and human-receptor research found that 11-OH-CBN reaches the brain and acts as a CB1 partial agonist, with potency and maximum activity approaching Delta-9-THC in one receptor assay. This suggests that 11-OH-CBN could contribute meaningfully to CBN’s effects after metabolism, although its independent psychoactive potency has not been established in humans.