MCPA targets broadleaf plants by mimicking the action of the plant hormone auxin (indole-3-acetic acid). This causes uncontrolled and abnormal growth, such as malformed leaves, stems, and roots, which is lethal to the plant. In addition to its auxin-mimicking activity, MCPA interferes with fundamental cellular processes in plants, including disrupting membrane integrity and energy metabolism by decreasing ATP levels, while also affecting the redox balance. In mammals, it has been shown to induce hepatic cytochrome P-450 levels.

In vitro, MCPA is primarily characterized for its herbicidal activity. Its activity is assessed by its ability to inhibit the growth of target weeds in controlled conditions. Additionally, in mammalian in vitro systems, MCPA has been shown to increase hepatic cytochrome P-450 levels and enhance the activities of aniline hydroxylase and 7-ethoxycoumarin O-deethylase. This indicates its potential to influence drug-metabolizing enzymes. It also interferes with membrane integrity and energy metabolism in plant cells.

In vivo, MCPA is a highly effective herbicide that is absorbed by plants and translocated throughout the system. Its primary effect is the death of susceptible broadleaf weeds, which is a result of the auxin-mimicking uncontrolled growth. While its in vivo activity is well-established for agricultural applications, it is also studied in animal models for its toxicological effects, as it can be absorbed by mammals and has been shown to increase hepatic cytochrome P-450 levels.

In vitro enzyme/receptor binding studies for MCPA are not typically performed in the context of pharmaceutical research, as it is an herbicide. However, its effects on mammalian enzyme systems have been studied. For instance, MCPA has been shown to increase hepatic cytochrome P-450 levels, which can be measured by assessing the activity of specific enzymes like aniline hydroxylase and 7-ethoxycoumarin O-deethylase in liver microsome preparations. This indicates its ability to interact with and induce metabolic enzymes.

In vitro cellular assays for MCPA are not standard for drug development, as it is an agricultural chemical. However, its toxicological effects can be studied in cell cultures. For example, its impact on membrane integrity and energy metabolism can be investigated by measuring ATP levels in treated plant or mammalian cells. Its potential to affect redox balance can also be assessed using cellular assays that measure oxidative stress markers. These assays help to characterize the compound's mechanism of action and toxicity at the cellular level.

In vivo animal studies for MCPA are conducted to assess its toxicological profile. In mammals, it has been shown to be orally active. Studies have demonstrated that MCPA increases hepatic cytochrome P-450 levels and enhances the activity of liver enzymes such as aniline hydroxylase. This suggests it can induce metabolic enzymes. These studies typically involve administering MCPA to rodents and then measuring the enzyme activities in liver homogenates. The primary in vivo activity, however, remains its herbicidal effect in plants.

Absorption, Distribution and Excretion
…Almost no absorption through the skin… /2,4-D/
(14)C MCPA…Intravenously injected into pregnant mice, followed by autoradiography studies every 5 minutes to 72 hours. The distribution pattern was characterized by high blood concentrations within 4 hours of injection and accumulation in the visceral yolk sac epithelium within 24 hours. The radioactive material crossed the placenta, but fetal tissues never reached the concentrations found in maternal tissues. The radioactive material was cleared from both fetal and maternal bodies within 24 hours of injection. After administration via gastric tube to rats, the highest concentrations of (14)C MCPA in tissues were reached within 2–8 hours, then rapidly decreased. Within the first 24 hours, 92.3% of the dose was detected in urine and 6.8% in feces. Approximately 50% of the total dose was detected in the urine of four volunteers within 48 hours of each ingesting 5 mg of MCPA. Five days after ingestion, the concentration in urine was below detectable levels of 0.02 ppm. For more complete data on the absorption, distribution, and excretion of 2-methyl-4-chlorophenoxyacetic acid (8 metabolites in total), please visit the HSDB record page. Metabolites/Metabolites: 4-chloro-2-hydroxymethylphenoxyacetic acid and N-(4-chloro-2-methylphenoxyacetyl)-L-aspartic acid are produced in rapeseed and wild carrot. 4-chloro-2-methylphenoxyacetyl-β-D-glucose may be produced in rapeseed. /Excerpt from Table/ 2-methyl-4-chlorophenol has been detected in cow milk and in the kidneys of sheep and cattle. Arthrobacter sp. and Flavobacterium peregrinum degrade MCPA to 4-chloro-2-methylphenol. Flavobacterium peregrinum further oxidizes the phenol, releasing all chloride ions. Aspergillus niger van Tiegh can also metabolize MCPA to 4-chloro-2-methyl-5-hydroxyphenoxyacetic acid. Gram-negative soil bacteria can metabolize MCPA to 5-chloro-o-cresol, which is believed to be 6-hydroxy-MCPA and α-methyl-γ-carboxymethyl-δ-α-butenolide. For more complete data on the metabolism/metabolites of 2-methyl-4-chlorophenoxyacetic acid (a total of 6 metabolites), please visit the HSDB record page. CDDs can be absorbed via oral, inhalation, and skin contact routes. CDDs are carried in plasma by serum lipids and lipoproteins and are mainly distributed in the liver and adipose tissue. CDDs are slowly metabolized into polar metabolites by the microsomal monooxygenase system, which can bind to glucuronic acid and glutathione. They can 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)
Pharmacokinetic properties of MCPA are characterized by its oral activity in mammals. It has a molecular weight of 200.62 g/mol and a chemical formula of C₉H₉ClO₃. As a phenoxy herbicide, it is absorbed and distributed in plants and animals. In mammals, it is metabolized and excreted, and its induction of cytochrome P-450 enzymes is a key aspect of its metabolic profile. It is generally used as a salt or ester to enhance its absorption and efficacy.

Toxicological data for MCPA indicate that it can have impacts on non-target organisms and the environment. In mammals, it has been shown to induce hepatic cytochrome P-450 levels and increase the activity of certain liver enzymes. It is also suspected to interact with the aryl hydrocarbon receptor, potentially altering gene transcription. As a herbicide, its toxicity to broadleaf plants is its primary effect, while its effects on mammals are a subject of safety assessments for agricultural workers and consumers.

[1]. Sorption and desorption of glyphosate, MCPA and tetracycline and their mixtures in soil as influenced by phosphate. J Environ Sci Health B. 2017 Dec 2;52(12):887-895.

[2]. Biodegradable PBAT/PLA Blend with Bioactive MCPA-PHBV Conjugate Suppresses Weed Growth. Biomacromolecules. 2018 Feb 12;19(2):511-520.

(4-Chloro-2-methylphenoxy)acetic acid is a chlorophenoxyacetic acid formed by substituting a methyl group at the 2-position of (4-chlorophenoxy)acetic acid. It can be used as a synthetic auxin, an environmental pollutant, and a phenoxy herbicide. It is a chlorophenoxyacetic acid belonging to the monochlorobenzene class of compounds. 2-Methyl-4-chlorophenoxyacetic acid (MCPA) is a potent, selective, and widely used phenoxy herbicide. It effectively controls broadleaf weeds, including thistle and sorrel, in cereal crops and pastures. It is selective for broadleaf plants, including most deciduous trees. Clover is tolerant at moderate application rates. Currently, it is listed as a restricted-use pesticide in the United States. A potent herbicide used as a selective herbicide.
MCPA is a widely used phenoxy herbicide that has been a key tool in agriculture for decades. It is also known by its IUPAC name, (4-chloro-2-methylphenoxy)acetic acid. Its selectivity for broadleaf weeds over monocotyledonous crops makes it valuable for cereal production. It is generally used as salts or esters and is available for research purposes to study its herbicidal action and toxicological effects. It is not a pharmaceutical agent.

C9H9CLO3

200.61

200.024

94-74-6

MCPA-d3;352431-14-2;MCPA-13C8

7204

Light yellow to yellow solid powder

1.3±0.1 g/cm3

327.0±27.0 °C at 760 mmHg

114-118 °C(lit.)

151.6±23.7 °C

0.0±0.7 mmHg at 25°C

1.552

2.49

1

3

3

13

184

0

WHKUVVPPKQRRBV-UHFFFAOYSA-N

InChI=1S/C9H9ClO3/c1-6-4-7(10)2-3-8(6)13-5-9(11)12/h2-4H,5H2,1H3,(H,11,12)

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

Raphone; Krezone; MCPA

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 : ~50 mg/mL (~249.23 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (12.46 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (12.46 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.)