Absorption, Distribution and Excretion
Overall recovery of metsulfuron methyl among the treatment groups was acceptable (about 91.6-103.8%). The primary route of excretion /in rats/ was via the urine which accounted for approximately 71-95% (78-96% if cage wash radioactivity is considered) among the various treatment groups. Fecal elimination was 4.8-13.3%. Excretion was almost complete within 48 ours. Based on time course urinary and fecal excretion data, elimination half-lives (males and females) were estimated to be 13-16 hours for Group I (single low dose), 9-12 hours for Group II (21 day dietary exposure), and 23-29 hours for Group III single high dose) which affirmed notable alteration of absorption and/or excretion processes in the high-dose group. Tissue burdens were minimal (generally <0.1% to 1%) regardless of exposure protocol; the gastrointestinal tract, carcass, and skin had the highest concentrations of radioactivity. For the single or repeated low dose groups, the tissue content was generally >0.03 ppm. In the high-dose group, females had somewhat higher tissue burdens (ranging from 0.8 ppm in brain to 7.1 ppm in liver and 8.0 ppm in kidneys) than did males (0.1 ppm in blood to 1.6 ppm in liver and 2.6 ppm in kidneys). No evidence for sequestration of the test article or its biotransformation products.
In mammals, following oral administration, metsulfuron-methyl is excreted predominantly unchanged. The methoxycarbonyl and sulfonylurea groups are only partly degraded, by O-demethylation and hydroxylation.

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Metabolism / Metabolites
Four metabolites and parent were recovered in both urine and feces /of rats/ in all treatment groups. Parent compound accounted for most of the urinary and fecal radioactivity (77-90% and 1.8-6.2% of the administered dose, respectively). Metabolite I was consistent with (methyl 2-((amino)sulfonyl)benzoate); Metabolite II - (2-((amino)sulfonyl)benzoic acid); and Metabolite III was consistent with (methyl 2-((((amino)carbonyl)amino)sulfonyl)benzoate). Metab. I and II appeared to result from sequential hydrolysis reactions terminating in the formation of saccharin while metab. III was formed by cleavage of the two ring structures. Total metabolites (in urine + feces of each group) accounted for approximately 5.4-8.2% of the administered dose. The metabolite profiles were qualitatively similar for urine and feces in that parent compound and the four metabolites (saccharin, metabolites I, II, and III) were found in both matrices.
(Phenyl-(U)-(14)C)sulfometuron-methyl was metabolized in excised wheat seedlings (sensitive to sulfometuron-methyl) to (14)C methyl 2-(((((4-hydroxymethyl)-6-methylpyrimindin-2-yl)amino)carbonyl)amino sulfonyl)benzoate and its carbohydrate conjugate. This metabolic pathway is consistent with sulfometuron-methyl metabolism in tolerant species such as Bermuda grass. Sulfometuron-methyl was metabolized at a slower rate than metsulfuron-methyl in wheat. When plants were exposed to (14)C methyl-4-hydroxy-2(((((4-methoxy-6-methyl-1,3,5-triazin-2- yl-) amino)carbonyl)amino)-sulfonyl)benzoate and (14)C methyl 2-(((((4-hydroxymethyl)-6-methylpyrimindin-2-yl) amino)carbonyl)amino)sulfonyl)benzoate (the primary hydroxylated wheat metabolites of metsulfuron-methyl and sulfometuron-methyl, respectively), the rate of glucose conjugation of methyl-4-hydroxy-2(((((4-methoxy-6-methyl- 1,3,5-triazin-2-yl-)amino)carbonyl)amino)-sulfonyl)benzoate was much faster than the rate of glucose conjugation of methyl 2-(((((4-hydroxymethyl)-6- methylpyrimindin-2- yl)amino)carbonyl)amino)sulfonyl)benzoate. Along with their parent cmpd, both methyl 2-(((((4-hydroxymethyl)-6- methylpyrimindin-2- yl)amino)carbonyl)amino)sulfonyl)benzoate and methyl-4-hydroxy-2(((((4-methoxy-6-methyl-1,3,5-triazin-2- yl- )amino)carbonyl)amino)-sulfonyl)benzoate are potent inhibitors of wild mustard acetolactate synthase. These results indicate that wheat intolerance to sulfometuron-methyl (but tolerance to the structurally closed related metsulfon-methyl) reflects not only a reduced ability to hydroxylate the parent molecule but also a reduced ability to conjugate the primary toxic metabolite to a nontoxic moiety.
In mammals, following oral administration, metsulfuron-methyl is excreted predominantly unchanged. The methoxycarbonyl and sulfonylurea groups are only partly degraded, by O-demethylation and hydroxylation.

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Biological Half-Life
Based on time course urinary and fecal excretion data /in rats/, elimination half-lives (males and females) were estimated to be 13-16 hours for Group I (single low dose), 9-12 hours for Group II (21 day dietary exposure), and 23-29 hours for Group III single high dose) ...

Toxicity Data
LC50 (rat) > 5,000 mg/m3/4h

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Non-Human Toxicity Values
LC50 Rat (male and female) inhalation >5 mg/L air/4 hr
LD50 Rat (male and female) oral >5000 mg/kg
LD50 Rabbit percutaneous >2000 mg/kg
LD50 Rabbit (male and female) oral >2000 mg/kg

Metsulfuron methyl is a N-sulfonylurea in which the sulfonyl group is attached to a 2-(methoxycarbonyl)phenyl group while a (4-methoxy-6-methyl-1,3,5-triazin-2-yl group replaces one of the amino hydrogens of the remaining urea group. It has a role as a herbicide, an environmental contaminant and a xenobiotic. It is a benzoate ester, a N-sulfonylurea and a methoxy-1,3,5-triazine.
Metsulfuron-methyl is a residual sulfonylurea herbicide that kills broadleaf weeds and some annual grasses. It is a systemic compound with foliar and soil activity, that inhibits cell division in shoots and roots. It has residual activity in soils, allowing it to be used infrequently but requiring up to 22 months before planting certain crops (sunflowers, flax, corn, or safflower). It has very low toxicity to mammals, birds, fish, and insects, but is a moderate eye irritant.

C14H15N5O6S

381.36

381.074

74223-64-6

52999

White crytals
White to pale yellow solid
Colorless crystals

1.473 g/cm3

647.2ºC at 760 mmHg

158°C

345.2ºC

1.593

2.03

2

9

6

26

609

0

CC1=NC(NC(OC)=N1)=NC(NS(=O)(C2=CC=CC=C2C(OC)=O)=O)=O

RSMUVYRMZCOLBH-UHFFFAOYSA-N

InChI=1S/C14H15N5O6S/c1-8-15-12(18-14(16-8)25-3)17-13(21)19-26(22,23)10-7-5-4-6-9(10)11(20)24-2/h4-7H,1-3H3,(H2,15,16,17,18,19,21)

methyl 2-[(4-methoxy-6-methyl-1,3,5-triazin-2-yl)carbamoylsulfamoyl]benzoate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~262.22 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.56 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.56 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)