Mecoprop (6.25 and 62.5 μM) raises the concentrations of estradiol (6.25 μM) and ketone (62.5 μM) in the oocytes' major myocardium [1].

Absorption, Distribution and Excretion
Male and female Wistar rats with dosed orally with (14)C-Mecoprop-P (radiochemical purity: 99.5%, purity: 98.6%; spec. act.: 138.8 uCi/mg). Five rats/sex were dosed with 5 (Groups A, B, D) or 100 mg/kg (Groups C and E). The rats in Group B received 14 doses of unlabeled Mecoprop-P (purity: 99.8%) at 5 mg/kg/day prior to being dosed with the radiolabeled material. In addition,12 rats/sex were dosed with 5 mg/kg (Group F). In Groups A, B and C, urine and feces were collected for 7 days. Expired air was collected from two males in Group C. In Groups D and E, blood samples were collected for 7 days. In Group F, four animals/sex/timepoint were euthanized at 0.5, 3 and 6 hours after dosing. Absorption of the administered dose ranged from 82.92 to 100.47% with the absorption minimally reduced in the repeated dosing regimen and at the higher dosing level (males: A. 100.47%, B. 94.58%, C. 92.34%; females: A. 94.62%, B. 92.07%, C. 82.92%). Excretion was predominantly via the urine with the percentage of the total dose recovered in the urine and cage wash ranging from 79.74 to 100.06%. In Group A, 95.29 and 92.29% of the administered dose was collected in the urine and the cage wash within the first 24 hours for males and females, respectively. Repeated dosing reduced the amount collected in the urine and the cage wash during the first 24 hours to 88.97 and 86.46% for males and females, respectively. Likewise, at the 100 mg/kg dosing level, the percentage collected in the urine and the cage wash during the first 24 hours was reduced to 61.18 and 56.78% for males and females, respectively. The total radiolabel recovered in the feces ranged from 3.56 to 12.52% of the administered dose. No radiolabeled material was recovered in the expired air due to the positioning of the label on the phenyl ring. Radiolabel in the tissues and organs 7 days after dosing was predominantly in the fat followed by the skin, adrenals, kidneys and liver. Maximal levels of radioactivity were recovered from the various tissues and organs assayed within 3 hours of dosing (Group F). In the plasma pharmacokinetic analysis, Tmax values were 1.8 and 2.7 hours for males and females, respectively in Group D and 4.2 hours in Group E. /The half-life/ for elimination was 6.35 and 4.23 hours in Group D and 7.89 and 7.79 hours in Group E for males and females, respectively. ... /Mecoprop-p/
Groups of 5 male Wistar rats were dosed orally with 5 mg/kg of either (14)C-Mecoprop-P-EHE (radiochemical purity: 99.6%, spec. act.: 145.37 uCi/mg) (Groups A and C) or (14)C-Mecoprop-P-DMA /(dimethylamine salt)/ (radiochemical purity (based on the acid): 99.8%, spec. act.: 114.79 uCi/mg) (Groups B and D). In Groups A and B (plasma pharmacokinetic study), blood samples were collected for 7 days. In Groups C and D, urine and feces were collected for 7 days. Expired air was collected for 48 hours. In the plasma pharmacokinetic analysis, Tmax values were 3.6 and 2 hr for Groups A and B, respectively. The half-life for elimination was 8.36 and 6.61 hours for Groups A and B, respectively. Absorption of the administered dose was at least 83.26 and 97.11% for Groups C and D, respectively (the total residual radiolabel in the tissues was not determined). Excretion was predominantly via the urine with the percentage of the total dose recovered in the urine 83.26 and 97.11%. In Groups C and D, respectively, 79.73 and 93.52% of the administered dose (calculated by the reviewer) was collected in the urine and the cage wash within the first 24 hours. The total radiolabel recovered in the feces was 3.29 and 4.68% of the administered dose for Groups C and D, respectively. No radiolabeled material was recovered in the expired air due to the positioning of the label on the phenyl ring. Radiolabel in the tissues and organs 7 days after dosing was largely limited to the skin and fat. The only metabolite identified in the study was hydroxymethyl-Mecoprop-P. Overall, unaltered test material and the hydroxylated metabolite constituted 96% of the recovered radiolabel in the first 48 hours after dosing. The parent material constituted 72.91 and 70.68% and the metabolite was 23.13 and 25.26% of the administered dose for Groups C and D, respectively.

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Metabolism / Metabolites
MCPP-p-DMAS (14)C-MCPP-p DMAS was incubated in vitro with rat plasma, stomach content, gastro-intestinal tract (GIT) or postmitochondrial liver fraction (S9) for 30 minutes. All incubated extracts were subjected to HPLC analysis. Results indicated that all of the administered (14)C-MCPP-p DMAS in plasma, stomach contents, gastro-intestinal tract and liver (S9) was present as the ionized form of (14)C-MCPP-p.
Male and female Wistar rats with dosed orally with (14)C-Mecoprop-P (radiochemical purity: 99.5%, purity: 98.6%; spec. act.: 138.8 uCi/mg). Five rats/sex were dosed with 5 (Groups A, B, D) or 100 mg/kg (Groups C and E). The rats in Group B received 14 doses of unlabeled Mecoprop-P (purity: 99.8%) at 5 mg/kg/day prior to being dosed with the radiolabeled material. In addition,12 rats/sex were dosed with 5 mg/kg (Group F). ... The only metabolite identified in the study was hydroxymethyl-Mecoprop-P. A greater percentage of this metabolite was recovered in the urine of the males. Overall, unaltered test material and the hydroxylated metabolite constituted 92.29 to 95.34% of the recovered radiolabel in the urine in the first 48 hours after dosing. For the males, the parent material was 52.17 to 67.08% and the metabolite was 28.26 to 41.39% of the administered dose. For the females these values ranged from 84.31 to 90.03% for the parent compound and 5.16 to 10.25% for the metabolite. /Mecoprop-p/
The dissociation of Mecoprop-p-DMA salt into Mecoprop-P acid and dimethyl amine was examined in various in vitro biological test systems. (14)C-Mecoprop-p-DMA was formed by mixing (14)C-Mecoprop-p acid (radiochemical purity: 99.5%, chemical purity: 98.6%, specific activity: 138.92 uCi/mg) with a dimethylamine solution. The test material was incubated with plasma (I), stomach contents (II), the gastrointestinal tract (III) and liver S9 fraction (IV) derived from male Wistar rats. The concentrations of the test material in the incubations were 0.1 (I), 5 (II), 0.35 (III) and 0.1 (IV) mg/mL. The samples were incubated for 30 minutes at 37o C. Study results indicated that the test material had largely dissociated into Mecoprop-P acid and DMA. It was not apparent from these results whether the dissociation may have been wholly or partially mediated enzymatically.
In ...plants, degradation of the side-chain to 2-methyl-4-chlorophenol, ring hydroxylation and ring opening.
CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing CDDs induce both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the feces, though smaller amounts are excreted in the urine and via lactation. (L177)

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Biological Half-Life
Groups of 5 male Wistar rats were dosed orally with 5 mg/kg of either (14)C-Mecoprop-P-EHE (radiochemical purity: 99.6%, spec. act.: 145.37 uCi/mg) (Groups A and C) or (14)C-Mecoprop-P-DMA (radiochemical purity (based on the acid): 99.8%, spec. act.: 114.79 uCi/mg) (Groups B and D). ... The half-life for elimination was 8.36 and 6.61 hours for Groups A and B, respectively. ...
/In/ two cases of serious intoxication with phenoxy herbicides (MCPP) ... The plasma half-life was about 17 hr. MCPP plasma elimination probably follows first-order kinetics.

Toxicity Summary
IDENTIFICATION AND USE: Mecoprop (MCPP) is a solid. It is used as an herbicide. HUMAN STUDIES: In two cases of serious intoxication with MCPP, both patients had central nervous system involvement, became unconscious and had an inadequate respiration. Muscle cramps and rhabdomyolysis with renal failure were noted in both. Shortly after admission both patients developed a serious decrease in arterial blood pressure (160/80 mmHg to 80/45 mmHg). In one patient this was demonstrated to be caused by a reduction in peripheral vascular resistance. In another case, a patient who had ingested 500 mL of a mecoprop product died of hypotension and respiratory failure 36 hours after hospital admission. Two additional cases of MCPP ingestion followed a similar clinical course with rapid loss of consciousness, muscle cramps, and hypotension. Laboratory abnormalities included decreased platelets and hemoglobin and elevated creatine phosphokinase and myoglobin levels. One patient also developed acute renal failure secondary to rhabdomyolysis and required hemodialysis. In surviving patients, no long-term effects were reported. In male human blood lymphocytes, chromosomal aberrations were increased in the presence of activation at a cytotoxic dosing level of 2500 ug/mL. ANIMAL STUDIES: In rats, MCPP caused structural changes in spleen and thymus and changes of the number of blood lymphocytes and granulocytes. In a carcinogenicity study in mice, MCPP was administered in the diet at doses of 4, 40, and 592 mg/kg/day for males and 4, 46, and 732 mg/kg/day for females. In females, an increase in the incidence of chronic nephropathy and increased absolute and relative kidney weight were reported. There was no treatment related increase in tumor incidence compared to controls in this study. MCPP was given orally to mice at days 6-15 of pregnancy. It was embryotoxic at doses greater than or equal to 300 mg/kg and caused malformations of the skeleton at doses greater than or equal to 400 mg/kg. Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 were exposed in the presence and absence of activation to MCPP at concentrations of 0, 50, 150, 500, 1500, and 5000 ug/plate with incubation for 3 days with a repeat assay. An increase in the reversion frequency was not indicated. ECOTOXICITY STUDIES: MCPP injured shell formation with an increase of shell abnormalities following herbicide concentrations in two larval stages of marine mollusk Crassostrea gigas. However, the toxic concentrations were several orders of magnitude higher than environmental concentrations. MCPP was nontoxic to bees.
CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. This includes 2,3,7,8-tetrachlorodibenzo-p-dioxin's carcinogenicity is thought to be the result of its ability to alter the capacity of both exogenous and endogenous substances to damage the DNA by inducing CYP1A1- and CYP1A2-dependent drug-metabolizing enzymes. (L177)

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Interactions
/The authors/ investigated the developmental toxicity in mice of a commercial formulation of herbicide containing a mixture of 2,4-dichlorophenoxyacetic acid, mecoprop, dicamba and inert ingredients. Pregnant mice were exposed to one of four different doses of the herbicide mixture diluted in their drinking water, either during preimplantation and organogenesis or only during organogenesis. Litter size, birth weight and crown-rump length were determined at birth. Dams were sacrificed by carbon dioxide asphyxiation and the number of implantation sites was determined by staining with ammonium sulfide. The data, although apparently influenced by season, showed an inverted or u-shaped dose response pattern for reduced litter size, with the lowest dose - which corresponds to the reference dose for 2,4-D - producing the greatest decrease in the number of embryos implanted and number of pups being born. Fetotoxicity, as evidenced by a decrease in weight and crown-rump length of the newborn pups was not significantly different in herbicide-treated litters.

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Non-Human Toxicity Values
LD50 Rabbit dermal 900 mg/kg
LD50 Mouse oral 369 mg/kg
LD50 Rat ip 402 mg/kg
LD50 Rat oral 650 mg/kg
For more Non-Human Toxicity Values (Complete) data for Mecoprop (6 total), please visit the HSDB record page.

[1]. Orton F, et al. Endocrine disrupting effects of herbicides and pentachlorophenol: in vitro and in vivo evidence. Environ Sci Technol. 2009 Mar 15;43(6):2144-50.

Mecoprop appears as colorless crystals. Corrosive to metals. Used as an herbicide.
2-(4-chloro-2-methylphenoxy)propanoic acid is a monocarboxylic acid that is lactic acid in which the hydroxyl hydrogen is replaced by a 4-chloro-2-methylphenyl group. It is an aromatic ether, a monocarboxylic acid and a member of monochlorobenzenes. It is functionally related to a rac-lactic acid.
Mecoprop, or methylchlorophenoxypropionic acid (MCPP), is a common general use herbicide found in many household weed killers and weed-and-feed type lawn fertilizers. It is primarily used to control broadleaf weeds. It is often used in combination with other chemically related herbicides such as 2,4-D, dicamba, and MCPA.The United States Environmental Protection Agency has classified mecoprop as toxicity class III - slightly toxic. Mecoprop is a mixture of two stereoisomers, with the (R)-(+)-enantiomer ('Mecoprop-P', 'Duplosan KV') possessing the herbicidal activity
See also: Mecoprop-P (annotation moved to).

C10H11CLO3

214.64

214.039

93-65-2

Mecoprop-d3;352431-15-3

7153

Colorless crystals
Solid

1.3±0.1 g/cm3

331.9±27.0 °C at 760 mmHg

88-90ºC

154.5±23.7 °C

0.0±0.8 mmHg at 25°C

1.542

2.84

1

3

3

14

208

0

O=C(C(C)OC1C(C)=CC(Cl)=CC=1)O

WNTGYJSOUMFZEP-UHFFFAOYSA-N

InChI=1S/C10H11ClO3/c1-6-5-8(11)3-4-9(6)14-7(2)10(12)13/h3-5,7H,1-2H3,(H,12,13)

2-(4-chloro-2-methylphenoxy)propanoic acid

Mecprop; Mecoturf; Mecoprop

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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