HI 6 has been shown to be efficacious in soman intoxication of laboratory animals by reactivation of acetylcholinesterase. To assess possible risks involved in the administration of HI 6 its degradation products were analyzed at pH 2.0, 4.0, 7.4, and 9.0. At pH 2.0, where HI 6 in aqueous solution has its maximal stability, attack on the aminal-acetal bond of the "ether bridge" predominates, with formation of formaldehyde, isonicotinamide, and pyridine-2-aldoxime. Besides, HI 6 decomposes at the oxime group yielding 2-cyanopyridine. Liberation of hydrocyanic acid at pH 2.0 is below 5%. At pH 7.4, primary attack is on the oxime group, resulting in formation of the corresponding pyridone via an intermediate nitrile. The pyridone has been isolated and identified as 2-pyridinone, 1-[(4-carbamoylpyridinio)methoxy)methyl)formate. This major metabolite deaminates further to the 2-pyridinone, 1-[(4-carboxypyridinio)methoxy)methyl) derivative, which ultimately decomposes into formaldehyde, isonicotinic acid, and 2-pyridone. Hydrolysis of the acid amide group probably also occurs with HI 6 itself. Significant amounts of free hydrocyanic acid were only detected in the presence of an alkali trap; otherwise hydrocyanic acid reacts with formaldehyde to yield hydroxyacetonitrile from which hydrocyanic acid can be liberated again. Up to 0.6 equivalents of hydrocyanic acid were evolved at pH 7.4. After repetitive administration and impaired renal elimination of HI 6, e.g. during renal shock, there might be some risk of cyanide intoxication.