Deuterated mitragynine
Pharmaceutical compound
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Deuterated mitragynine (developmental code name KUR-101) is an atypical μ-opioid receptor agonist and deuterated analogue of mitragynine (found in kratom) which is under development for the treatment of acute pain and opioid-related disorders.[2][3][1][4][5] It is taken by mouth.[1][2] Deumitragynine is said to have analgesic effects.[4] The drug is being developed by ATAI Life Sciences and Kures.[2][3][1][5] As of December 2022, it is in phase 1 clinical trials for acute pain and opioid-related disorders.[2][3][1]
Other namesDeu-mitragynine; Deuterated mitragynine; KUR-101; KUR101
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"KUR 101". AdisInsight. 27 December 2022. Retrieved 26 February 2025. Cano GH, Dean J, Abreu SP, Rodríguez AH, Abbasi C, Hinson M, et al. (December 2022). "Key Characteristics and Development of Psychoceuticals: A Review". International Journal of Molecular Sciences. 23 (24) 15777. doi:10.3390/ijms232415777. PMC 9779201. PMID 36555419. S2CID 254672601. Table 1. Biochemical structures, mechanisms, and receptor functions of twenty psychoceutical drugs: [...] Drug Name: Deu-mitragynine (Kratom) [...] Chemical Structure: *. Target Type: Opioid Receptor. Method of Action: Deu-mitragynine acts as a mu-opioid (MOR) agonist with the ability to interact with G-protein coupled receptors, resulting in its analgesic effects. Deu-mitragynine has been shown to exhibit opioid-receptor-dependent analgesic effects and G-protein-based agonists of MOR. Citations: Atai Life Sciences [28] Shukla et al. [29] [...] The drugs targeting opioid receptors, deu-mitragynine (a major alkaloid component of kratom [28]) and salvinorin A (a non-alkaloidal component of Salvia divinorum [30]), regulate pathways initiated by G-proteins, while also stimulating other mechanisms, such as the beta-arrestin and ERK/MAPK pathways. Kratom, a mu-opioid receptor (MOR) agonist with low potency, has been demonstrated to emit 'atypical' opioid effects (no respiratory depression, emesis, or shortness of breath in animal models) through G-protein agonistic activity and limited recruitment of beta-arrestin after opioid receptor-dependent activation [28,29]. Studies with rodent models alternatively suggest mitragynine and its derivatives do not directly activate opioid receptors [29], which brings into question how the drug initiates the activity of MORs to deliver analgesic effects.
