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Research tools

DO34

A laboratory probe that blocks DAGLs and lowers brain 2-AG in mice.

Unscheduled
Level of detail

Harm-reduction warning

No characterised human dose: animal / in vitro data only. Effect profile, safety margin and acute toxicity are not documented in human clinical practice. Extremely potent compound: severe effects, seizures and deaths reported in the literature.

C₂₆H₂₈F₃N₅O₄

CID 129188708

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
531.50 g/mol

Updated on

In plain terms

DO34 is not a cannabinoid from hemp: it is a laboratory tool created to cut the production of 2-AG, one of the cannabinoids the body makes itself. In mice, injecting this molecule lowers 2-AG in the brain within hours. It is used only for research; it is not a consumer product.

Receptors and activity

Target network

CB1Binding (function not established)no measured value
  • Blocks or inhibits
  • Binds or modulates

The lower the cited value, the closer the target sits to DO34: one ring per factor of 100. A target with no measured value stays on the edge.

Where these targets live

Where each target has been found in humans, according to the cited studies. The map shows the target, not an effect of DO34.

Brain, side view
Body, front view
Blood

CB1CB1 found in 7 regions of the body

  1. Basal gangliadenseMost dense in basal ganglia outflow nuclei1
  2. CerebellumdenseVery dense in the cerebellum1
  3. HippocampusdenseVery high concentrations in the hippocampus2
  4. AmygdaladenseHigh concentrations in the amygdala2
  5. CortexpresentPresent throughout the neocortex2
  6. Adipose tissuepresentExpressed in adipose tissue3
  7. GutpresentColonic epithelium, smooth muscle and plexus4

Map sources

  1. Herkenham M et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A, 1990 (new tab)
  2. Glass M et al. Cannabinoid receptors in the human brain: a detailed anatomical and quantitative autoradiographic study in the fetal, neonatal and adult human brain. Neuroscience, 1997 (new tab)
  3. Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
  4. Wright K et al. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology, 2005 (new tab)

Cited values

  1. DAGLαInhibitorIC50 = 6 nM · human70 out of 100

    Ogasawara et al., PNAS 2016 (new tab) · recombinant human DAGLα (HEK293T cell lysates), conversion of the SAG substrate to 2-AG; 95% confidence interval of 3 to 11 nM

  2. DAGLβInhibitorno measured value cited
  3. PLA2G7Inhibitorno measured value cited
  4. ABHD6Inhibitorno measured value cited
  5. CB1Binding (function not established)no measured value cited
Bar length follows the measured value (Ki, Kd, EC50 or IC50), on one scale shared by every entry, from 100 µM to 0.1 nM. A target with no cited value has no bar.

Pharmacology

DO34 is a 1,2,3-triazole urea, a chemical probe of the endocannabinoid system. It does not bind CB1 and CB2 to any notable extent (IC50 above 1 µM) but covalently and irreversibly inhibits diacylglycerol lipases α and β, which produce 2-arachidonoylglycerol: IC50 of 6 nM on recombinant human DAGLα and 3 to 8 nM on DAGLβ (Ogasawara et al. 2016). In mice, intraperitoneal injection of 3 to 50 mg/kg blocked brain DAGLα in a dose-dependent manner (ED50 of 5 to 10 mg/kg, full inhibition at 30-50 mg/kg); within 2 h, 2-AG, anandamide, arachidonic acid and the prostaglandins PGD2 and PGE2 fell while the precursor diacylglycerols accumulated. In brain slices, 0.1 to 1 µM DO34 almost fully blocked depolarisation-induced suppression of excitation (DSE) in the cerebellum and of inhibition (DSI) in the hippocampus, two CB1-dependent forms of synaptic plasticity. In mice, DO34 also impaired extinction of a learned fear (Cavener et al. 2018) and delayed acquisition in the Morris water maze, with lower 2-AG and arachidonic acid and a higher diacylglyceride precursor in several brain regions (Schurman et al. 2019). DAGLs are not its only targets (PLA2G7, ABHD6), hence the use of the control DO53. All these data are preclinical.

Key sources.

History

Source
A synthetic molecule of the 1,2,3-triazole urea class, absent from cannabis and from any living organism. A chemical probe used in laboratory pharmacology to suppress 2-AG production.

Origin

Research tool

No biosynthetic pathway: a synthetic molecule of the 1,2,3-triazole urea class.

Classification

Family, origin and source verification

Family

ECS pharmacological tool › Enzyme inhibitor

Verification

Classification, sources and binding values checked on 20 October 2026; text read against its sources and Wikipedia.

Wikipedia (English)

No dedicated article.

References

  1. Ogasawara D et al., Rapid and profound rewiring of brain lipid signaling networks by acute diacylglycerol lipase inhibition, PNAS 2016;113(1):26-33 (new tab)PMID 26668358
  2. Deng H et al., Triazole Ureas Act as Diacylglycerol Lipase Inhibitors and Prevent Fasting-Induced Refeeding, Journal of Medicinal Chemistry, 2017 (new tab)PMID 27992221
  3. Cavener VS et al., Inhibition of Diacylglycerol Lipase Impairs Fear Extinction in Mice, Frontiers in Neuroscience 2018 (new tab)PMID 30108473
  4. Schurman LD et al., Diacylglycerol Lipase-Alpha Regulates Hippocampal-Dependent Learning and Memory Processes in Mice, Journal of Neuroscience 2019 (new tab)PMID 31127001
  5. ANSM, Consolidated list of substances classified as narcotics, updated 16 February 2026, annex IV (new tab)
  6. PubChem, DO34, CID 129188708 (formula and identifiers) (new tab)

Identifiers

Names

IUPAC name
tert-butyl 3-benzyl-4-[4-[4-(trifluoromethoxy)phenyl]triazole-1-carbonyl]piperazine-1-carboxylate
Other names
DO-34

Identifiers

Formula
C₂₆H₂₈F₃N₅O₄
PubChem CID
129188708(new tab)
InChIKey
CQGMWUWJVBKTRM-UHFFFAOYSA-N
SMILES
CC(C)(C)OC(=O)N1CCN(C(C1)CC2=CC=CC=C2)C(=O)N3C=C(N=N3)C4=CC=C(C=C4)OC(F)(F)F

Machine-readable entry (JSON)

LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.