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 were orally administered (14) C-Mecoprop-P (radiochemical purity: 99.5%, purity: 98.6%; specific activity: 138.8 μCi/mg). Five male and five female rats in each group were given 5 mg/kg (groups A, B, and D) or 100 mg/kg (groups C and E), respectively. Group B rats were given unlabeled Mecoprop-P (purity: 99.8%) at a dose of 5 mg/kg/day for 14 consecutive days before receiving the radiolabeled substance. Additionally, 12 male and 12 female rats in group F were given 5 mg/kg. Urine and feces were collected from rats in groups A, B, and C for 7 consecutive days. Exhaled air was collected from two male rats in group C. Blood samples were collected from rats in groups D and E for 7 consecutive days. In group F, four animals of each sex at each time point were sacrificed 0.5, 3, and 6 hours after administration. The absorption rate of the administered dose ranged from 82.92% to 100.47%, with a slight decrease at repeated dosing and higher dose levels (males: Group A 100.47%, Group B 94.58%, Group C 92.34%; females: Group A 94.62%, Group B 92.07%, Group C 82.92%). The drug was primarily excreted in the urine, with the percentage of total dose recovered in urine and cage flushing fluid ranging from 79.74% to 100.06%. In Group A, 95.29% and 92.29% of the administered dose were collected from urine and cage flushing fluid in males and females, respectively, within 24 hours post-dosing. Repeated dosing reduced the radioactive material content collected in urine and cage flushing fluid within 24 hours post-dosing to 88.97% in males and 86.46% in females, respectively. Similarly, at a dose level of 100 mg/kg, the levels of radioactive material collected in urine and cage flushing fluid decreased to 61.18% in males and 56.78% in females within 24 hours after administration. The total amount of radiolabeled material recovered in feces ranged from 3.56% to 12.52% of the administered dose. No radiolabeled material was detected in exhaled breath due to the label being located on the benzene ring. Seven days after administration, the radiolabeled material in tissues and organs was primarily found in adipose tissue, followed by skin, adrenal glands, kidneys, and liver. Maximum levels of radioactivity recovered from various tissues and organs were reached within 3 hours after administration (Group F). In plasma pharmacokinetic analysis, the Tmax values for male and female rats in Group D were 1.8 hours and 2.7 hours, respectively, and for Group E, it was 4.2 hours. The elimination half-lives for male and female rats in Group D were 6.35 hours and 4.23 hours, respectively, and for Group E, they were 7.89 hours and 7.79 hours, respectively. Five male Wistar rats were randomly divided into two groups and orally administered 5 mg/kg of (14)C-Mecoprop-P-EHE (radiochemical purity: 99.6%, specific activity: 145.37 μCi/mg) (groups A and C) or (14)C-Mecoprop-P-DMA (dimethylamine salt) (radiochemical purity (acid-based): 99.8%, specific activity: 114.79 μCi/mg) (groups B and D). Blood samples were collected from groups A and B (plasma pharmacokinetic studies) for 7 consecutive days. Urine and fecal samples were collected from groups C and D for 7 consecutive days. Exhaled breath samples were collected for 48 hours. Plasma pharmacokinetic analysis showed that the time to peak concentration (Tmax) was 3.6 hours for group A and 2 hours for group B. The elimination half-lives were 8.36 hours for group A and 6.61 hours for group B. The absorption rates of the administered dose in groups C and D were at least 83.26% and 97.11%, respectively (total residual radiolabeled substances in tissues were not determined). The drug was primarily excreted in the urine, with 83.26% and 97.11% of the total dose recovered in urine, respectively. 79.73% and 93.52% of the administered dose (calculated by the reviewer) in groups C and D were recovered from urine and cage cleaning fluid within 24 hours post-administration. The total amount of radiolabeled substances recovered in feces in groups C and D was 3.29% and 4.68% of the administered dose, respectively. No radiolabeled substances were recovered from exhaled breath due to the label being located on the benzene ring. Seven days after administration, radiolabeled substances in tissues and organs were primarily found in the skin and fat. The only metabolite identified in this study was hydroxymethyl-methoxypropionic acid-P. Overall, 96% of the radiolabeled substances recovered within 48 hours post-administration were unchanged test substances and hydroxylated metabolites. In groups C and D, the parent material accounted for 72.91% and 70.68% of the administered dose, respectively, while metabolites accounted for 23.13% and 25.26% of the administered dose, respectively.

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Metabolites/Metabolites
MCPP-p-DMAS (14)C-MCPP-p DMAS was incubated in vitro with rat plasma, gastric contents, gastrointestinal tract (GIT), or mitochondrial-to-liver fraction (S9) for 30 minutes. All incubated extracts were analyzed by HPLC. The results showed that all administered (14)C-MCPP-p DMAS in plasma, gastric contents, gastrointestinal tract, and liver (S9) were in the ionized form of (14)C-MCPP-p.
Male and female Wistar rats were orally administered (14)C-Mecoprop-P (radiochemical purity: 99.5%, purity: 98.6%; specific activity: 138.8 μCi/mg). Five male and five female rats in each group were administered 5 mg/kg (groups A, B, and D) or 100 mg/kg (groups C and E), respectively. Group B rats received unlabeled Mecoprop-P (purity: 99.8%) at a dose of 5 mg/kg 14 times daily before receiving the radiolabeled substance. Additionally, twelve male and twelve female rats in each group received 5 mg/kg (group F). …The only metabolite identified in this study was hydroxymethyl-Mecoprop-P. A higher proportion of this metabolite was recovered in the urine of males. Overall, within 48 hours post-administration, 92.29% to 95.34% of the radiolabeled substance recovered in urine were unchanged test substances and hydroxylated metabolites. For males, the maternal substance accounted for 52.17% to 67.08% of the administered dose, and the metabolites accounted for 28.26% to 41.39%. For women, these values for the parent compound ranged from 84.31% to 90.03%, and for the metabolites from 5.16% to 10.25%. /Mecoprop-p/
The dissociation of Mecoprop-p-DMA salts into Mecoprop-P acid and dimethylamine was investigated in various in vitro bioassay systems. (14)C-Mecoprop-p-DMA was prepared by mixing (14)C-Mecoprop-p acid (radiochemical purity: 99.5%, chemical purity: 98.6%, specific activity: 138.92 μCi/mg) with a dimethylamine solution. The test substance was incubated with plasma (I), gastric contents (II), gastrointestinal tract (III), and liver S9 fraction (IV) from male Wistar rats, respectively. The concentrations of the test substance in the incubation solutions were 0.1 (I), 5 (II), 0.35 (III), and 0.1 (IV) mg/mL, respectively. The sample was incubated at 37°C for 30 minutes. The results showed that the test substance was largely dissociated into mecoprop-p acid and DMA. It is unclear from these results whether the dissociation was complete or partially enzymatically mediated. In plants, the side chain degrades to 2-methyl-4-chlorophenol, undergoing cyclohydroxylation and ring-opening reactions. Chlorodibenzo-p-dioxins (CDDs) can be absorbed via oral, inhalation, and skin contact. CDDs are carried in plasma by lipids and lipoproteins, and are mainly distributed in the liver and adipose tissue. CDDs are metabolized very slowly in the microsomal monooxygenase system, producing polar metabolites that can bind to glucuronic acid and glutathione. They may increase their metabolic rate by inducing phase I and phase II enzymes. The main excretion routes of CDDs are bile and feces, with small amounts also excreted through urine and lactation. (L177)

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Biological Half-Life
Five male Wistar rats were divided into four groups and orally administered 5 mg/kg of (14)C-Mecoprop-P-EHE (radiochemical purity: 99.6%, specific activity: 145.37 uCi/mg) (groups A and C) or (14)C-Mecoprop-P-DMA (radiochemical purity (acid-based): 99.8%, specific activity: 114.79 uCi/mg) (groups B and D). …The elimination half-lives for groups A and B were 8.36 hours and 6.61 hours, respectively. …In two cases of severe phenoxy herbicide (MCPP) poisoning…the plasma half-life was approximately 17 hours. Plasma elimination of MCPP likely follows first-order kinetics.

Toxicity Summary
Identification and Uses: Methoxypropionic acid (MCPP) is a solid used as a herbicide. Human Studies: In two severe cases of MCPP poisoning, both patients presented with central nervous system involvement, loss of consciousness, and respiratory failure. Both patients also experienced muscle spasms, rhabdomyolysis, and renal failure. Shortly after admission, both patients developed a severe drop in arterial blood pressure (from 160/80 mmHg to 80/45 mmHg). In one patient, the drop in blood pressure was confirmed to be due to decreased peripheral vascular resistance. The other patient died 36 hours after admission from hypotension and respiratory failure following the ingestion of 500 mL of MCPP. Two other cases of MCPP ingestion presented with similar clinical courses, including rapid loss of consciousness, muscle spasms, and hypotension. Laboratory abnormalities included decreased platelet and hemoglobin levels, and elevated creatine phosphokinase and myoglobin levels. One patient also developed acute renal failure secondary to rhabdomyolysis and required hemodialysis. No long-term effects were reported in surviving patients. Chromosomal aberrations were increased in male peripheral blood lymphocytes at a cytotoxic dose of 2500 μg/mL. Animal studies: In rats, MCPP caused structural changes in the spleen and thymus, as well as changes in the number of blood lymphocytes and granulocytes. In a mouse carcinogenicity study, male mice were administered MCPP by diet at doses of 4, 40, and 592 mg/kg/day, respectively, while female mice were administered MCPP at doses of 4, 46, and 732 mg/kg/day, respectively. An increased incidence of chronic kidney disease, with increases in both absolute and relative kidney weight, was reported in female mice. No increased tumor incidence was observed in the treatment group compared to the control group in this study. Mice were orally administered MCPP on days 6–15 of gestation. MCPP exhibited embryotoxicity at doses ≥300 mg/kg; MCPP caused skeletal malformations at doses ≥400 mg/kg. With or without activation, Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 were exposed to MCPP at concentrations of 0, 50, 150, 500, 1500, and 5000 μg/plate for 3 days, and the experiments were repeated. No increase in reversal frequency was observed. Ecotoxicity studies: MCPP impaired shell formation in both larval stages of the marine mollusc Crassostrea gigas and led to increased shell deformity rates after treatment with different concentrations of MCPP. However, its toxic concentrations were several orders of magnitude higher than environmental concentrations. MCPP is non-toxic to bees. CDDs exert toxic effects by binding to aromatic hydrocarbon receptors, thereby altering the transcription of certain genes. The affinity for aromatic hydrocarbon receptors depends on the structure of the specific CDD. Alterations in gene expression may be due to direct interactions between aryl hydrocarbon receptors and their heterodimer-forming partners—aryl hydrocarbon receptor nuclear transposons—and gene regulatory elements, or to the initiation of a phosphorylation/dephosphorylation cascade that activates other transcription factors. Affected genes include a variety of oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. These alterations in gene transcription/translation are considered the cause of much of the toxicity of CDDs. This includes the carcinogenicity of 2,3,7,8-tetrachlorodibenzo-p-oxins, which is thought to be due to their ability to alter the ability of exogenous and endogenous substances to damage DNA by inducing CYP1A1 and CYP1A2-dependent drug-metabolizing enzymes. (L177)

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Interactions
/Authors/Studied the developmental toxicity of a commercial herbicide formulation containing a mixture of 2,4-dichlorophenoxyacetic acid, methoxypropionic acid, dicamba, and an inert ingredient in mice. Pregnant mice were exposed to four different doses of the herbicide mixture dissolved in drinking water, either pre-implantation and during organogenesis or only during organogenesis. Litter size, birth weight, and crown-rump length were measured at birth. Mothers were euthanized by carbon dioxide asphyxiation, and the number of implantation sites was determined by ammonium sulfide staining. Although the data were significantly affected by season, the results showed an inverted U-shaped dose-response curve for reduced litter size, with the lowest dose (equivalent to the reference dose of 2,4-D) resulting in the largest decrease in implantation and birth numbers. The decrease in newborn weight and crown-rump length in the herbicide-treated groups indicated no significant difference in fetal toxicity.

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Non-human toxicity values
Rabbit dermal LD50: 900 mg/kg
Mice oral LD50: 369 mg/kg
Rat intraperitoneal LD50: 402 mg/kg
Rat oral LD50: 650 mg/kg
For more non-human toxicity values (complete data) for methoxypropionic acid (6 items), 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.

Methylchloropropionic acid is a colorless crystalline solid, corrosive to metals, and used as a herbicide. 2-(4-chloro-2-methylphenoxy)propionic acid is a monocarboxylic acid, a structure in which the hydroxyl hydrogen in lactic acid is replaced by 4-chloro-2-methylphenyl. It is an aromatic ether, a monocarboxylic acid, and belongs to the monochlorobenzene class of compounds. Its function is similar to racemic lactic acid. Methylchloropropionic acid, also known as methylchlorophenoxypropionic acid (MCPP), is a common general-purpose herbicide found in many household herbicides and 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 U.S. Environmental Protection Agency classifies methylchloropropionic acid as Group III – slightly toxic. Dicamba is a mixture of two stereoisomers, in which the (R)-(+)-enantiomer (“dicamba-P”, “duprosanne KV”) has herbicidal activity. See also: Dicamba-P (note 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.)