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Imazapyr is an analytical standard used for proteomics research.

ChEBI: 2-(4-isopropyl-4-methyl-5-oxo-4,5-dihydro-1H-imidazol-2-yl)nicotinic acid is a pyridinemonocarboxylic acid that is nicotinic acid which is substituted at position 2 by a 4,5-dihydro-imidazol-2-yl group, which in turn is substituted at positions 4, 4, and 5 by isopropyl, ethyl, and oxo groups, respectively. It is a member of pyridines, a member of imidazolines, an imidazolone and a pyridinemonocarboxylic acid.

Imazapyr kills plants by inhibiting acetolactate synthase (ALS) (I50 = 5 μM), which is the first common enzyme in the biosynthesis of the branched chain amino acids, valine, leucine, and isoleucine. Imazapyr is rapidly absorbed through the leaves of plants. Once it enters the plant, imazapyr rapidly translocates to the growing points and growth ceases within 1 day after herbicide application followed by chlorosis and then necrosis of the growing points. Total plant death will occur within 2 to 3 weeks after treatment.

Imazapyr is weakly to moderately adsorbed on sandy loam and silt loam soils. The Freundlich adsorption coefficient ranges from 0 to 7.8 (15). Because imazapyr is a weak acid and exists in different ionic states, soil pH has an effect on soil binding properties. The anionic form predominates at soil pH as low as 5.5, and this form bindsweakly to soil. The neutral or molecular form is important at soil pH from 4 to 6.5. This form binds to soil organic matter and clay. The cationic form is important at pH less than 4. Because the soil is a heterogeneous mixture of acid and base chemical groups, there may be sites within a particular soil that are 2 to 3 pH units higher or lower than the average pH. The cationic form will bind tightly to the lower pH components. Because of these interactions, small decreases in pH below 6 will result in large increases in binding. The half-life of imazapyr in the soil is 25–142 d (14). Imazapyr remains in the top 30 cm of the soil with low leaching potential. The degradation route of imazapyr in the soil has not been determined.

Plant Metabolism. The selectivity of imazapyr is due to differential rates and routes of metabolism in tolerant crops versus susceptible weeds (3). The half-life of imazapyr in tolerant crops has not been accurately determined. The metabolic route of imazapyr is not clear. The parent compound can be metabolized to a tricyclic compound (33, Fig. 15) in some species, but the primary metabolite is an imidazopyrrolo-pyridine derivative (34, Fig. 15). This compound does not inhibit acetolactate synthase, the target site for the imidazolinones, and it is immobile in the plant (4).
Animal Metabolism. Metabolism studies in the rat showed that imazapyr is rapidly excreted in the urine (5). There was no accumulation of imazapyr or any of its derivatives in the liver, kidney, muscle, fat, or blood.

Imazapyr has shown no mutagenic or genotoxic activity in the Ames assay, mammalian cell gene mutation assay, in vitro chromosome aberration assay, in vitro unscheduled DNA synthesis (URS) assay, or the in vivo dominant lethal assay in male rats.This herbicide also has a low potential for bioaccumulation in fish.