Chemical Properties
Off-White Solid
Uses
Imazamox is an imidazolinone based acetolactate synthase inhibitor that is utilized as a herbicide for weed control.
Definition
ChEBI: 2-(4-isopropyl-4-methyl-5-oxo-4,5-dihydro-1H-imidazol-2-yl)-5-(methoxymethyl)nicotinic acid is a pyridinemonocarboxylic acid that is nicotinic acid which is substituted substituted at position 5 by a methoxymethyl group and at position 2 by a 4,5-dihydro-1H-imidazol-2-yl group, that in turn is substituted by isopropyl, methyl, and oxo groups at positions 4, 4, and 5, respectively. It is a pyridinemonocarboxylic acid, an ether, an imidazolone and a member of imidazolines.
Production Methods
The industrial synthesis of imazamox begins with the construction of its imidazolinone core, typically through condensation reactions involving pyridine carboxylic acid derivatives and imidazolinone intermediates. The process includes key steps such as cyclization to form the heterocyclic ring and selective substitution to introduce functional groups that enhance herbicidal activity. Esterification or salt formation may be employed to improve solubility and formulation stability. Reaction conditions, such as temperature, solvent choice, and pH, are carefully optimised to maximise yield and purity while minimising environmental impact.
Mechanism of action
Contact and residual activity. Inhibits plant amino acid synthesis - acetohydroxyacid synthase AHAS.
Pharmacology
Imazamox kills plants by inhibiting acetolactate synthase
(ALS) (I50 = 1 μM), which is the first common enzyme in
the biosynthesis of the branched chain amino acids, valine,
leucine, and isoleucine. Imazamox is rapidly absorbed
through the leaves of plants. Once it enters the plant,
imazamox rapidly translocates to the growing points and
growth ceases within 1 day after herbicide application,
followed by chlorosis and then by necrosis of the growing
points. Total plant death will occur within 2 to 3 weeks
after treatment.
Metabolism
Plant Metabolism. The selectivity of imazamox is due to
differential rates and routes of metabolism in tolerant
crops versus susceptible weeds (10). The primary
metabolic route is hydroxylation followed by conjugation
to glucose. In imidazolinone-resistant crops, the primary
mechanism of selectivity is due to an altered acetolactate
synthase that is not inhibited by imazamox (11).
Animal Metabolism. Metabolism studies in the rat
showed that imazamox is rapidly excreted in the urine.
There was no accumulation of imazamox or any of its
derivatives in the liver, kidney, muscle, fat, or blood (9).
Toxicity evaluation
Imazamox 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 inmale rats. The acute toxicity and effects on wildlife
and soilmicroflora of imazamox are shown in Table 4. This
herbicide also has a low potential for bioaccumulation
in fish.
