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CP-55,940 is a synthetic non-classical cannabinoid that acts as a potent, non-selective full agonist at the CB1 and CB2 cannabinoid receptors. Developed by Pfizer in the 1970s during a search for cannabinoid-based analgesics, it lacks the classic tricyclic dibenzopyran ring of THC yet reproduces the full cannabinoid pharmacological profile with far greater potency. Its tritiated form, [3H]CP-55,940, became the standard radioligand used to detect, clone, and map cannabinoid receptors, making the compound a foundational reference tool in endocannabinoid research rather than a therapeutic or consumer product.
- Reference-grade full agonist for characterizing CB1 and CB2 pharmacology
- Tritiated form is the classic radioligand for locating and quantifying cannabinoid receptors
- Potent, dose-dependent analgesia in preclinical acute, inflammatory, and neuropathic pain models
- CB2-mediated antinociception can suppress neuropathic pain without central CB1 effects
- Roughly balanced CB1/CB2 affinity makes it a clean non-selective probe
- Strongly psychoactive and cannabimimetic through CB1 activation
- Tolerance develops with repeated dosing and can precipitate withdrawal
- Very high potency raises overdose and toxicity risk relative to THC
Overview
CP-55,940 is hands down one of the most important molecules in cannabinoid science; it is essentially the ruler that every new CB ligand gets measured against. Unlike THC, which only partially tugs on the receptor, this one is a clean full agonist at both CB1 and CB2, so it fully flips the switch; that potency is exactly why the tritiated version ([3H]CP-55,940) became the classic radioligand that let researchers find and map these receptors in the first place. Its value as a pharmacology reference point is hard to overstate; it is pretty much the gold standard for characterizing anything cannabinoid. Just keep it framed right; it is a potent research chemical and a lab reagent, not a supplement or a recreational product, and the CB1 side carries the usual cannabimimetic baggage.
Mechanism
CP-55,940 binds the orthosteric pocket of the cannabinoid CB1 and CB2 receptors (Gi/o-coupled GPCRs) with roughly equal, low-nanomolar affinity and acts as a full , meaning it drives the receptor to its maximal active conformation more completely than the partial agonist THC. Receptor activation exchanges GDP for GTP on the Gi/o alpha subunit, which inhibits adenylyl cyclase and lowers intracellular cyclic AMP; the released G-beta-gamma subunits then inhibit N- and P/Q-type voltage-gated calcium channels and open inwardly rectifying potassium (GIRK) channels.
At CB1 receptors on presynaptic terminals this dampens neurotransmitter release (retrograde signaling), producing analgesia, hypothermia, catalepsy, and the psychoactive/cannabimimetic effects; at CB2 receptors, concentrated on immune cells and , the same suppression drives anti-inflammatory and antinociceptive actions. Structurally it is a non-classical cannabinoid: it keeps the phenol and 1,1-dimethylheptyl side chain that anchor to the receptor but drops THC's pyran ring, and it also recruits beta-arrestin, contributing to receptor internalization and tolerance on repeated exposure.
receptor fingerprint
CB1 receptorFull agonist
CB2 receptorFull agonist
Adenylyl cyclase (via Gi/o)Inhibits
Voltage-gated Ca2+ channels (N-, P/Q-type)Inhibits
GIRK potassium channelsActivates
GPR55Modulates
Safetyrisks and cautions, not medical advice
CP-55,940 is a research chemical, not an approved drug or supplement, and has no established human safety data. As a full CB1 agonist it is far more potent than THC, so it reliably produces cannabimimetic effects, hypothermia, catalepsy, and motor impairment in animals, with tolerance and rimonabant-precipitated withdrawal on repeated dosing. Its high potency mirrors the toxicity risks seen with synthetic cannabinoid receptor agonists. It should be handled only as a laboratory reagent.
Subjective profileweighing the evidence above
A foundational, research-grade cannabinoid; invaluable as a laboratory probe and radioligand, but a potent CB1/CB2 full agonist that is not a consumer or therapeutic compound.
Resources
This entry is here for reference.
Research
- 1995first citedComparison of the pharmacology and signal transduction of the human cannabinoid CB1 and CB2 rec…
- 2025most recentIn vitro pharmacological activity of twenty-eight synthetic cannabinoid receptor agonists at th…
- 1.Comparison of the pharmacology and signal transduction of the human cannabinoid CB1 and CB2 receptors
- 2.Antinociceptive effects of the non-selective cannabinoid receptor agonist CP 55,940 are absent in CB1(-/-) and not CB2(-/-) mice in models of acute and persistent pain
- 3.CB1 Knockout Mice Unveil Sustained CB2-Mediated Antiallodynic Effects of the Mixed CB1/CB2 Agonist CP55,940 in a Mouse Model of Paclitaxel-Induced Neuropathic Pain
- 4.Structural basis of selective cannabinoid CB2 receptor activation
- 5.In vitro pharmacological activity of twenty-eight synthetic cannabinoid receptor agonists at the type 1 and 2 cannabinoid receptors
5 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
What is CP-55,940 used for?
Almost entirely as a research tool. Its tritiated form, [3H]CP-55,940, is the classic radioligand scientists use to detect, map, and quantify CB1 and CB2 cannabinoid receptors, and the unlabeled compound serves as a full-agonist reference standard for characterizing new cannabinoid ligands. It is not sold or used as a medicine or supplement.
How does CP-55,940 work?
It binds CB1 and CB2 receptors with roughly equal, low-nanomolar affinity and acts as a full agonist, activating Gi/o signaling that lowers cyclic AMP, inhibits calcium channels, and opens potassium channels. At CB1 this reduces neurotransmitter release and produces analgesia plus psychoactive effects; at CB2 it drives anti-inflammatory, immune-mediated pain relief.
Is CP-55,940 well-researched?
Yes, in the laboratory. It is one of the most heavily used cannabinoid reference compounds; foundational studies established its CB1 and CB2 binding affinities and knockout-mouse work has dissected which effects come from each receptor. What is missing is human clinical study, because it is a research reagent rather than a drug candidate.
How does CP-55,940 compare to THC?
It reproduces the same cannabinoid effects but is a full agonist and roughly an order of magnitude or more potent than THC, which is only a partial agonist. Structurally it lacks THC's central pyran ring, making it a non-classical cannabinoid, yet it still fully engages both receptor subtypes.
Is CP-55,940 safe to take?
No. It has no human safety data, is highly potent, and carries the toxicity and dependence risks associated with synthetic full cannabinoid agonists. It is intended only for laboratory research, not for human consumption.
Limitations of the evidence
- Produces hypothermia, catalepsy, and motor impairment in animal models
Adverse effects
- Strongly psychoactive and cannabimimetic through CB1 activation
- Tolerance develops with repeated dosing and can precipitate withdrawal
- Very high potency raises overdose and toxicity risk relative to THC
Notes and cautions
- Not approved or characterized for human therapeutic or recreational use