Chlorpropham (1-20 μM; 6 days) prevents D cells from proliferating. culture of salinity [2]. A six-day study using chloron (10 or 20 μM) revealed a rise in phytoene in D. salina cultures in the presence of red LED light [2].

Absorption, Distribution and Excretion
After oral or ip administration of (14)C isopropyl and (14)C ring-labelled chloropropham to rats, 4 day urinary excretions were 50 and 85% of dose, respectively for two sites of labelling; in case of isopropyl-labelled compound, an additional 17-20% of dose was excreted as CO2 via lungs. ...When pregnant rats were given (14)C chloropropham, radioactivity was readily transferred to fetuses, and its level did not decline in fetal tissues as rapidly as it did in maternal organs. Pups of lactating rats that were given labelled chloropropham also contained radioactivity.
In Wistar rats given single oral dose of labeled chlorpropham average urinary excretions of radioactivity were 55.9% and 82.6% of chain (14)C CIPC and ring (14)C CIPC. With chain CIPC 35.4 + or - 7.5% of administered dose was excreted in respired air.
Dermal absorption is not significant.
Chlorpropham or its metabolites are readily transported acropetally following root absorption and may be transported basipetally from foliar application in some plants. ...Polar metabolites are not translocated once they are formed in either roots or shoots.
For more Absorption, Distribution and Excretion (Complete) data for CHLORPROPHAM (7 total), please visit the HSDB record page.

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Metabolism / Metabolites
In rats, most important metabolic transformation of chloropropham is hydroxylation in the para-position and conjugation of the resulting 4-hydroxychloropropham with sulfate. Hydroxylation of the isopropyl residue accounts for about 1/3 of the metabolism of this herbicide. ...Approximately 4 times more monohydroxy compound than dihydroxy compound were detected. Compound undergoes further oxidation... hydrolytic fission... yields meta-chloroaniline, carbon dioxide and isopropanol, which is further oxidized to acetone and carbon dioxide. Hydroxylation of... meta-chloroaniline also takes place to give N-acetyl-4-amino-2-chlorophenol... plus N-acetyl-2-amino-4-chlorophenol... .
...It was... suggested that chlorpropham... metabolized differently between sensitive and resistant plants. ...Intact carbamates /found/ in sensitive plants... were not observed in resistant plant.
Hydrolysis of carbamate linkage occurred in neomycin treated rats, and in vitro investigation suggested that liver is site of hydrolysis.
Following oral administration... to rats, renal excretion was followed. ...Although the expected hydrolysis products were not found free, n-acetyl hydroxyl analogs were excreted and identified. The 1-carbethoxy compound and a metabolite believed to be 1-hydroxypropyl-2-n-(3-chloro-4-hydroxyphenyl) carbamate was found... after root treatment of soybean plants with CIPC, polar metabolites of CIPC from root and shoot tissues were isolated and purified. Data showed major root metabolite was o-glucoside of 2-hydroxy CIPC. This was also found in shoots... .
For more Metabolism/Metabolites (Complete) data for CHLORPROPHAM (15 total), please visit the HSDB record page.
The carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (L793)

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Biological Half-Life
...The average biological half-life of 14C from both compounds in most organs /of rats administered an oral dose of 14C-labelled propham or chloropropham/ was short, ranging from 3-8 hr. However, in brain, fat, and muscle, the half-life was about twice this value.

Toxicity Summary
Chlorpropham is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.

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Interactions
In order to investigate the various steps of chlorpropham metabolism which could be influenced by cadmium, isolated rat hepatocytes were incubated in the presence of chlorpropham (0.1 mM) and of increasing cadmium concn (0-180 uM). The results showed that cadmium accumulation in hepatocytes was in good correlation to its concn in the incubation medium. At 90 uM cadmium, hydroxylation of chlorpropham was only slightly decreased by 30%, while chlorpropham hydrolysis into 3-chloraniline was unaffected by the presence of cadmium. Accordingly, unchanged chlorpropham increased in hepatocytes. At 27 uM cadmium, free 4-hydroxychlorpropham increased in the intracellular medium as a consequence of a strong suppression of both sulfation and glucuronidation which was related to the strong depletion of the intracellular adenosine triphosphate level under the combined influences of both cadmium and free 4-hydroxychloropropham. Acetylation of 3-chloroaniline, which represents a minor pathway of chlorpropham metabolism, was already markedly suppressed (43%) with the lowest cadmium concn (27 uM). These in vitro results suggest that Phase II reactions are more sensitive to cadmium than Phase I processes and that cadmium enhanced the chloropropham cytotoxicity as shown by alterations of the membrane integrity.

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Non-Human Toxicity Values
LD50 Rabbit dermal >2000 mg/kg
LC50 Rat oral 1200 mg/kg
LD50 Rat ip 700 mg/kg
LD50 Mouse ip 2600 mg/kg
For more Non-Human Toxicity Values (Complete) data for CHLORPROPHAM (6 total), please visit the HSDB record page.

[1]. Göckener B, et al. Fate of Chlorpropham during High-Temperature Processing of Potatoes. J Agric Food Chem. 2020 Feb 26;68(8):2578-2587.
[2]. Yanan Xu, et al. Phytoene and phytofluene overproduction by Dunaliella salina using the mitosis inhibitor chlorpropham. Algal Research, Volume 52, December 2020, 102126.

Isopropyl-n-(3-chlorophenyl)carbamate is a brown chunky solid. (NTP, 1992)
Chlorpropham is a carbamate ester that is the isopropyl ester of 3-chlorophenylcarbamic acid. It has a role as a herbicide and a plant growth retardant. It is a carbamate ester, a member of benzenes and a member of monochlorobenzenes.
Chlorpropham is a carbamate pesticide. Carbamate pesticides are derived from carbamic acid and kill insects in a similar fashion as organophosphate insecticides. They are widely used in homes, gardens and agriculture. The first carbamate, carbaryl, was introduced in 1956 and more of it has been used throughout the world than all other carbamates combined. Because of carbaryl's relatively low mammalian oral and dermal toxicity and broad control spectrum, it has had wide use in lawn and garden settings. Most of the carbamates are extremely toxic to Hymenoptera, and precautions must be taken to avoid exposure to foraging bees or parasitic wasps. Some of the carbamates are translocated within plants, making them an effective systemic treatment. (L795)
A carbamate that is used as an herbicide and as a plant growth regulator.

C10H12CLNO2

213.66

213.055

101-21-3

Chlorpropham-d7;2140327-49-5

2728

Colorless solid
Light-tan powder
Light brown crystalline solid

1.2±0.1 g/cm3

251.1±23.0 °C at 760 mmHg

41°C

105.7±22.6 °C

0.0±0.5 mmHg at 25°C

1.561

3.49

1

2

3

14

197

0

ClC1=C([H])C([H])=C([H])C(=C1[H])N([H])C(=O)OC([H])(C([H])([H])[H])C([H])([H])[H]

CWJSHJJYOPWUGX-UHFFFAOYSA-N

InChI=1S/C10H12ClNO2/c1-7(2)14-10(13)12-9-5-3-4-8(11)6-9/h3-7H,1-2H3,(H,12,13)

propan-2-yl N-(3-chlorophenyl)carbamate

Mirvale; Metoxon; Chlorpropham

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.)