Contents

ADB-CHMINACA

Chemical compound

ADB-CHMINACA

Legal status
Legal status	BR: Class F2 (Prohibited psychotropics)[1] CA: Schedule II DE: Anlage II (Authorized trade only, not prescriptible) UK: Class B US: Schedule I UN: Psychotropic Schedule II[2] Illegal in Singapore, Sweden, Switzerland
Identifiers
IUPAC name N-[(2S)-1-Amino-3,3-dimethyl-1-oxobutan-2-yl]-1-(cyclohexylmethyl)indazole-3-carboxamide
CAS Number	1185887-13-1 Y
PubChem CID	68894304
ChemSpider	48059556
UNII	SL4C60689M
KEGG	C22698 Y
CompTox Dashboard (EPA)	DTXSID301016900
Chemical and physical data
Formula	C21H30N4O2
Molar mass	370.497 g·mol−1
3D model (JSmol)	Interactive image
SMILES CC(C)(C)[C@H](NC(=O)c1nn(CC2CCCCC2)c3ccccc13)C(N)=O
InChI InChI=1S/C21H30N4O2/c1-21(2,3)18(19(22)26)23-20(27)17-15-11-7-8-12-16(15)25(24-17)13-14-9-5-4-6-10-14/h7-8,11-12,14,18H,4-6,9-10,13H2,1-3H3,(H2,22,26)(H,23,27)/t18-/m1/s1 Key:ZWCCSIUBHCZKOY-GOSISDBHSA-N

ADB-CHMINACA (also known as ADMB-CHMINACA^[3] and MAB-CHMINACA) is an indazole-based synthetic cannabinoid. It is a potent agonist of the CB₁ receptor with a binding affinity of K_i = 0.289 nM and was originally developed by Pfizer in 2009 as an analgesic medication.^[4][5] It was identified in cannabinoid blends in Japan in early 2015.^[6]

There have been a number of reported cases of deaths and hospitalizations in relation to this synthetic cannabinoid.^{[7][8][9][10][11][12][13][14]}

In the United States, ADB-CHMINACA is a Schedule I controlled substance.^[15] Prior to its listing at the federal level in 2018, Louisiana placed ADB-CHMINACA on its Schedule I list by emergency scheduling in 2014.^[16]

Sweden's public health agency suggested to classify ADB-CHMINACA as hazardous substance on November 10, 2014.^[17]

ADB-CHMINACA is listed in the Fifth Schedule of the Misuse of Drugs Act (MDA) and therefore illegal in Singapore as of May 2015.^[18]

ADB-CHMINACA is illegal in Switzerland as of December 2015.^[19]

Ten ADB-CHMINACA major metabolites were identified in several incubations with cryopreserved human hepatocytes. Most transformations occurred at the cyclohexylmethyl tail of the compound.^[20]