MMB-FUBINACA is an analytical reference material categorized as a synthetic cannabinoid. 1. MMB-FUBINACA is regulated as a Schedule I compound in the United States. This product is intended for research and forensic applications.
AMB-FUBINACA (also known as FUB-AMB and MMB-FUBINACA) is an indazole-based synthetic cannabinoid that is a potent agonist for the cannabinoid receptors, with Ki values of 10.04 nM at CB1 and 0.786 nM at CB2 and EC50 values of 0.5433 nM at CB1 and 0.1278 nM at CB2,[1] and has been sold online as a designer drug.It was originally developed by Pfizer which described the compound in a patent in 2009, but was later abandoned and never tested on humans.
- 5F-AB-PINACA
- 5F-ADB
- 5F-AMB
- 5F-APINACA
- AB-CHFUPYCA
- AB-FUBINACA
- AB-PINACA
- ADB-CHMINACA
- ADB-FUBINACA
- ADB-PINACA
- ADSB-FUB-187
- APINACA
- MDMB-CHMICA
- MDMB-CHMINACA
- MDMB-FUBINACA
- PX-2
- PX-3
Synonyms
- AMB-FUBINACA
- FUB-AMB
Technical Information
- DMF: 30 mg/ml
- DMSO: 25 mg/ml
- Ethanol: 30 mg/ml
- Ethanol:PBS (pH 7.2)(1:2): 0.3 mg/ml
Shipping & Storage Information
Analysis of AMB-FUBINACA Biotransformation Pathways in Human Liver Microsome and Zebrafish Systems by Liquid Chromatography-High Resolution Mass Spectrometry
In this study, the metabolic profiles of a new illicit drug AMB-FUBINACA were investigated using both human liver microsome and zebrafish models.
Liquid chromatography Q Extractive HF Hybrid Quadrupole-Orbitrap mass spectrometry (LC-QE-HF-MS) was employed to analyze the metabolic sites and pathways. AMB-FUBINACA was added to the in vitro liver microsome incubation model to simulate the metabolic processes in human body.
The results showed that a total of 17 metabolites were generated in the human liver microsome model; the main metabolic pathways of the phase I metabolism included ester hydrolysis, methylation, ester hydrolysis combined with decarboxylation, hydroxylation, ester hydrolysis combined with indazole ring hydroxylation, etc.
while glucuronidation served as the main metabolic pathway of the phase II metabolism.