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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

The substance is an ester which undergoes acid and base catalyzed hydrolysis. Both the parent compound and the product of hydrolysis, HTMP (CAS 2403-88-5) are considered in this toxicokinetic assessment.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - oral (%):
Absorption rate - dermal (%):
Absorption rate - inhalation (%):

Additional information


The substance is an ester which undergoes acid and base catalyzed hydrolysis. Incubation of the substance at a concentration of 1 mg/L, pH 1 and 40°C for 24 h resulted in hydrolysis of 55% of the substance. Less than 10% hydrolysis was observed at pH 4. Ingestion will therefore result in at least some formation of HTMP (CAS 2403-88-5) and fatty acids in the stomach. As HTMP itself is a strong base, it will exist in a protonated form.

Substance that is not hydrolysed in the stomach may undergo non-enzymatic hydrolysis at the slightly basic pH in the duodenum and possibly also by enzymatic hydrolysis via bile enzymes.

Any parent substance is expected to exist to some extent in a protonated form because the nitrogen of the piperidine is a base. This increases solubility and it is predicted to be emulgated by bile acids and to be taken up and transported via chylomicrones. The substance is a surface-active fatty acid ester which is also an argument for uptake via the chylomicrones.

Considering the molecular weight, the liquid state and surface activity, uptake via the skin and via the lung is assumed. Dermal absorption appears to be lower or less critical since 2000 mg/kg bw caused mortality via the oral, but not via the dermal route.

Repeated oral dosing of the substance causes quite drastic effects on body weight gain during the first days. It is suspected that some sort of adaption regarding the mucous layer or xenobiotic metabolism induction is taking place. In the acute oral toxicity study, irritation of the gastrointestinal tract was seen at necropsy of the two animals that died after treatment (BASF 2013).



HTMP is highly water soluble and therefore expected to be found in the plasma. Accumulation in fat is not favoured by a log Pow of 0.24. The hazard profile of HTMP is dominated by local effects on the gastrointestinal tract that are considered to be caused by the corrosivity and the extreme pH. No specific target organ toxicity was observed neither for HTMP upon subacute or the substance itself at subchronic oral exposure.

The log Pow of the parent compound at pH 5.8 and 8 was measured to be greater than 6.5 and accumulation in fat is in theory possible. However, ester functions are known to be hydrolysed by non-specific esterases in the plasma. Due to hydrolysis the concentration of the parent compound in the body is not expected to be very high. Also for the parent compound the hazard profile is dominated by local effects on the mucous membranes, because the substance has a pH of 9.7 at a 10% suspension in water. Indeed, no specific effect indicating bioaccumulation was observed in the subchronic feeding study (BASF 2014).



Enzymatic and non-enzymatic ester hydrolysis results in formation of HTMP and a fatty acid. No experimental data is available regarding the metabolism of HTMP; however it is sufficiently soluble and small to be eliminated without further metabolism. Fatty acids are either incorporated into fat or degraded to carbon dioxide.



HTMP is expected to be rapidly eliminated via the kidney as it is a small molecule of high water solubility.