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
Following oral or intraperitoneal injection of 14C isopropyl and 14C ring-labeled chloramphenicol in rats, 50% and 85% of the administered dose were excreted in the urine after 4 days, respectively (both labeling sites). For the isopropyl-labeled compound, an additional 17-20% of the dose was excreted via the lungs as CO2. …When pregnant rats were administered 14C chloramphenicol, the radioactive material readily transferred to the fetus, and its level in fetal tissues decreased less rapidly than in maternal organs. Pups of lactating rats also contained radioactivity after administration of labeled chloramphenicol. In Wistar rats, the mean urinary excretion of radioactive material following a single oral dose of labeled chloramphenicol was 55.9% and 82.6% of that of chain 14C-CIPC and cyclic 14C-CIPC, respectively. 35.4 ± 7.5% of the administered dose of chain CIPC was excreted via respiration. Dermal absorption was not significant. Chloramphenicol or its metabolites are readily transported upwards after absorption in the roots, and in some plants, downwards after foliar application. Polar metabolites, once formed in the roots or stems, are no longer transported. For more complete data on the absorption, distribution, and excretion of chloramphenicol (7 types), please visit the HSDB record page. Metabolism/Metabolites In rats, the most important metabolic transformations of chloramphenicol are para-hydroxylation and the binding of the resulting 4-hydroxychloroamphenicol to sulfate. Hydroxylation of isopropyl residues accounts for approximately one-third of the metabolism of this herbicide. The amount of monohydroxy compounds detected was approximately four times that of dihydroxy compounds. Further oxidation of the compounds…hydrolysis and cleavage…generates m-chloroaniline, carbon dioxide, and isopropanol. Isopropanol is further oxidized to acetone and carbon dioxide. The hydroxylation of m-chloroaniline also produces N-acetyl-4-amino-2-chlorophenol and N-acetyl-2-amino-4-chlorophenol.
Studies have shown that chloropropamine is metabolized differently in susceptible and resistant plants. The intact carbamate found in susceptible plants was not observed in resistant plants.
Hydrolysis of the carbamate bonds occurred in rats treated with neomycin, and in vitro studies showed that the liver was the site of hydrolysis.
Renal excretion was tracked after oral administration to rats. Although the expected free hydrolysis products were not found, N-acetylhydroxy analogs were detected and identified. Following treatment of soybean plant roots with chloropropane (CIPC), a 1-ethoxycarbonyl compound and its metabolite were discovered, which was identified as 1-hydroxypropyl-2-n-(3-chloro-4-hydroxyphenyl)carbamate. Polar metabolites of CIPC were isolated and purified from root and stem tissues. Data showed that the major metabolite in roots was O-glucoside of 2-hydroxyCIPC. This metabolite was also found in stems. For more complete data on the metabolites/metabolites of chloropropane (15 in total), please visit the HSDB record page. Carbamates are enzymatically hydrolyzed in the liver; degradation products are excreted via the kidneys and liver. (L793)

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Biological half-life
…In most organs, the mean biological half-life of both compounds at 14C was short (in rats after oral administration of 14C-labeled propylamine or chloropropane), ranging from 3 to 8 hours. However, in the brain, fat, and muscle, the half-life is about twice that value.

Toxicity Summary
Chlorpromazine is a cholinesterase, or acetylcholinesterase (AChE) inhibitor. Carbamate compounds form unstable complexes with cholinesterase by carbamylation of the enzyme's active site. This inhibition is reversible. Cholinesterase inhibitors suppress the activity of acetylcholinesterase. Because acetylcholinesterase has important physiological functions, chemicals that interfere with its activity are potent neurotoxins, causing excessive salivation and lacrimation even at low doses. High-dose exposure typically results in symptoms such as headache, salivation, nausea, vomiting, abdominal pain, and diarrhea. Acetylcholinesterase breaks down the neurotransmitter acetylcholine, which is released at the neuromuscular junction, causing muscle or organ relaxation. Inhibition of acetylcholinesterase results in the accumulation and sustained action of acetylcholine, leading to continuous nerve impulse transmission and uninterrupted muscle contraction.

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Interaction
To investigate the potential effects of cadmium on various steps of chloroamphetamine metabolism, isolated rat hepatocytes were incubated in the presence of chloroamphetamine (0.1 mM) and increasing concentrations of cadmium (0–180 μM). The results showed a strong correlation between cadmium accumulation in hepatocytes and its concentration in the incubation medium. At a cadmium concentration of 90 μM, hydroxylation of chloroamphetamine was reduced only slightly by 30%, while the hydrolysis of chloroamphetamine to 3-chloroaniline was unaffected by cadmium. Consequently, the content of unmetabolized chloroamphetamine in hepatocytes increased. At a cadmium concentration of 27 μM, intracellular levels of free 4-hydroxychloroamphetamine were elevated due to strong inhibition of both sulfation and glucuronidation. This inhibition was associated with a significant decrease in intracellular adenosine triphosphate (ATP) levels under the combined effects of cadmium and free 4-hydroxychloroamphetamine. The secondary pathway of chloroamphetamine metabolism—acetylation of 3-chloroaniline—was also significantly inhibited (43%) at the lowest cadmium concentration (27 μM). These in vitro results indicate that the Phase II response was more sensitive to cadmium than the Phase I response, and that cadmium enhanced the cytotoxicity of chloramphenicol, manifested as alterations in cell membrane integrity.

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Non-human toxicity values
Rabbit dermal LD50 >2000 mg/kg
Rats oral LC50 1200 mg/kg
Rats intraperitoneal LD50 700 mg/kg
Mouse intraperitoneal LD50 2600 mg/kg
For more non-human toxicity values (complete data) for chloramphenicol (6 in 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, lumpy solid. (NTP, 1992) Chloramphenicol is a carbamate, the isopropyl ester of 3-chlorophenylcarbamic acid. It is used as a herbicide and plant growth inhibitor. It is a carbamate, belonging to the benzene and monochlorobenzene compounds. Chloramphenicol is a carbamate insecticide. Carbamate insecticides are derived from carbamic acid, and their insecticidal mechanism is similar to that of organophosphate insecticides. They are widely used in homes, gardens, and agriculture. The first carbamate insecticide, Sevin, was introduced in 1956, and its global usage exceeds that of all other carbamate insecticides combined. Due to its relatively low oral and dermal toxicity to mammals and its broad spectrum of application, Sevin is widely used in lawns and gardens. Most carbamate herbicides are highly toxic to hymenopteran insects, and precautions must be taken to avoid contact with insects such as bees or parasitic wasps. Some carbamate herbicides can be transported within plants and are therefore effective systemic herbicides. (L795)
A carbamate herbicide used as both a herbicide and 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.)