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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

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In vitro the metabolism of DMAPN to cyanide, formaldehyde and cyanoacetic acid was localized mostly in the microsomal fraction of liver, kidney and urinary bladders. Presumably DMAPN is primarily metabolized via a cytochrome P450-dependent mixed-function oxidase system.The biochemical effects of DMAPN included depletion of glutathione and increased lipid peroxidation in target organs, including urinary bladder and kidney. Studies indicate that there are species differences in the toxicity spectrum of DMAPN metabolites (Mumtaz et al. 1991a, 1991b). Froines et al. (1985a) identified cyanide, formaldehyde (in vitro) and thiocyanate (in vivo) as metabolites.

Acetylcholin esterase (AChE) was inhibited by all the aminonitriles tested in a concentration-dependent manner (Froines et al. 1985b). DMAPN did not inhibit monoamine oxidase (MAO) activity in rat brain or liver in vivo (Wilmarth & Froines 1991).


Rats treated with 525 mg/kg bw twice on one day with DMAPN or equimolar doses of commercially available potential DMAPN metabolites showed varying levels of urinary retention. About 44% of the administered dose of DMAPN was excreted unchanged in 5 days, while mice excreted only about 6% of the dose. ß-Aminopropionitrile and cyanoacetic acid were identified as urinary metabolites. In vitro, cyanide, formaldehyde and cyanoacetic acid were identified as metabolites (Mumtaz et al. 1991a, 1991b).