Prometryn targets the photosynthetic electron transport chain in plants, specifically inhibiting photosystem II. By binding to the D1 protein of the photosystem II complex, it blocks the transfer of electrons, thereby inhibiting photosynthesis. This leads to the death of susceptible weeds. It does not have a target in animals or humans, but its herbicidal activity is mediated through this specific interaction in plants.

In vitro, Prometryn is used as a standard in analytical chemistry for the identification and quantification of the herbicide in various samples. It is also used in studies of herbicide resistance and the mechanism of action of photosystem II inhibitors. The compound's herbicidal activity is assessed in plant-based assays, where it inhibits photosynthesis and causes weed death. It does not have significant pharmacological activity in animal cells.

Prometryn is not a pharmacologically active compound in animals and therefore does not have defined in vivo activity as a therapeutic agent. It is a herbicide used in agriculture. When administered to animals, it would likely be metabolized and excreted. Its primary value is as an agricultural chemical and as an analytical standard for residue analysis in food and environmental samples.

In vitro assays for Prometryn are primarily analytical, using techniques such as gas chromatography (GC) or high-performance liquid chromatography (HPLC) coupled with mass spectrometry for its detection and quantification in samples. These methods are used to monitor prometryn residues in food and environmental samples. Enzyme-linked immunosorbent assays (ELISAs) may also be developed for its detection.

In vitro cellular assays using Prometryn are not commonly performed, as it is a herbicide with no significant activity in animal cells. However, it may be used in ecotoxicological studies to assess its effects on non-target organisms, such as algae or aquatic plants, where it inhibits photosynthesis. These studies are used to evaluate the environmental impact of the herbicide.

In vivo animal studies with Prometryn are conducted to assess its toxicity and environmental fate. A typical protocol involves administering the compound to rodents or other test animals and monitoring for adverse effects. These studies are used to determine the compound's toxicity profile, metabolic pathways, and potential for bioaccumulation. They are part of the regulatory requirements for pesticide registration.

Absorption, Distribution and Excretion
Following administration of hundreds of mg/kg of unlabeled simazine, atrazine, promethazine, prazole, and prazole to rats and rabbits, monoalkylated and dialkylated parent compounds were detected in urine. In rats, most of the administered prazole was excreted in urine and feces within 48 hours. When the substance labeled with 14C was administered to rats by gavage, 2,4-bis(isopropylamino)-6-methylthio-triazine was detected in both urine and feces. This chemical is absorbed and rapidly excreted. Small amounts have been reported to transfer to the milk of lactating goats or the eggs of laying hens. Triazine compounds, including prazole, are generally well absorbed by the mammalian intestine and may also be absorbed through the skin. The breakdown process of propamidin is not fully understood… No residues of propamidin or its metabolites were detected in the muscle, fat, blood, liver, kidneys, or other organs of sheep and cattle fed with concentrations up to 100 ppm propamidin for 4 weeks. However, propamidin or its breakdown products were detected in whole milk samples from dairy cows fed with concentrations up to 100 ppm propamidin for 21 days. They are readily absorbed by the intestines and are presumably also absorbed through the skin and lungs. /Urea, uracil, and triazine herbicides/

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Metabolism/Metabolites
In addition to the -OH substitution of the CH3S- group, in rats and rabbits treated with atrazine, the CH3S- group undergoes dealkylation without sulfur oxidation, followed by oxidative coupling to form disulfides.
...When cotton, soybeans, peanuts, and carrots were treated with atrazine labeled with a 14C ring, hydroxypromethazine and hydroxyatrazine were detected...Studies of peas treated with atrazine labeled with 14CH3 provided supporting evidence for methyl thiolysis, in which a suitable amount of 14C carbon dioxide was released.
Rats and rabbits fed atrazine excreted 2-mercapto-4-amino-6-isopropylamino-triazine and bis(2-amino-4-isopropylamino-triazinyl-6-yl) disulfide. Mono- and di-dealkylated atrazine analogs were also observed. Eight-day-old pea seedlings were exposed to...and harvested after eight days. The results indicated the existence of multiple metabolic pathways. In one pathway, the side chain of atrazine was metabolized, and 2-hydroxy-4-amino-6-isopropylamino-triazine was identified. In another pathway, the methyl sulfide group is oxidized to a sulfone, which is readily hydrolyzed to a hydroxyl analog. Chromatographic analysis revealed the presence of sulfoxides and hydroxyl analogs. In rats and rabbits, atrazine is converted into thio derivatives and their corresponding disulfides, as well as many other urinary metabolites. For more complete metabolite/metabolite data on atrazine (a total of 8 metabolites), please visit the HSDB record page.
Prometryn is absorbed and distributed in the body after administration. It is metabolized and excreted primarily in the urine and feces. The compound's pharmacokinetic properties have been studied in the context of its toxicity and environmental fate. It has a relatively short half-life in animals and is not expected to accumulate significantly.

Toxicity Summary
Pyromazine was first registered in the United States in 1964 for use as a herbicide against weeds in cotton, celery, pigeon pea, and dill fields. The registration standard was published in March 1987 (NTIS# PB87-184826)... In laboratory animal studies, the toxicity of pyromazine technical via oral, dermal, and inhalation routes was assessed as mild to almost non-toxic, thus classifying it as Toxicity Category III (second lowest of four categories). Furthermore, the toxicity of pyromazine technical for acute eye irritation and skin irritation was also assessed as mild to almost non-toxic, thus classifying it as Toxicity Category III and IV, respectively. Pyromazine is not considered a sensitizer. A 28-day subchronic rat feeding study showed macroscopic and microscopic pathological changes in the high-dose group, limited to the gastrointestinal tract, along with clinical symptoms and significant weight loss. A 21-day rabbit dermal toxicity study showed no local or systemic toxicity observed at the highest dose (1000 mg/kg/day). Three chronic toxicity/carcinogenicity studies in mice, rats, and dogs respectively indicated that pyrimidine was not carcinogenic. Because pyrimidine did not alter the spontaneous tumor profile of the tested mouse and rat strains, it was classified as a Group E carcinogen (no evidence of carcinogenicity in humans). However, the results from the canine study were not considered because, although some effects were observed under the study conditions, these effects were not carcinogenic. A developmental toxicity study in rats showed that the highest dose resulted in maternal and developmental toxicity. Another study, also in rabbits, showed adverse reactions including increased abortion rate and weight loss in the highest dose group. A two-generation reproductive study in rats showed adverse reactions including weight loss and correspondingly reduced food consumption in the highest dose group. However, significant weight loss in pups (also in the high-dose group) was considered toxicologically significant because it could negatively impact postnatal development of systems such as the nervous and immune systems. In four mutagenicity studies (Amssalmonella assay, chromosome aberration assay, bacterial DNA repair assay, and unplanned DNA synthesis assay), chlormequat was negative for mutagenicity. A series of (radiolabeled) general metabolic studies in rats showed that chlormequat was primarily distributed in the blood, followed by the spleen, and lastly the lungs. Humans may be exposed to chlormequat residues through diet. Permissible or maximum residue limits have been established for various crops and animal products…

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Toxicity Data
LC50 (rat) = 5,170 mg/m3/4h

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Interactions
When used in combination with simazine in lactating rats, postpartum effects reported on days 5 to 10 at unspecified doses included decreased body weight, reduced neuromuscular maturity, and stunted physical development.

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Non-human toxicity values
Oral LD50 in rats: 5233 mg/kg /Technical grade/
Oral LD50 in rats: 3750 mg/kg /80% wettable powder/
Oral LD50 in rats: 3150 mg/kg
Oral LD50 in rats, (male) 1802 (1265-2568) mg/kg, (female) 2076 (1654-2607) mg/kg
For more complete non-human toxicity data for PROMETRYNE (11 in total), please visit the HSDB records page.
Prometryn has been shown to have toxic effects in animals at high doses. It may cause irritation to the skin, eyes, and respiratory tract. It is classified as a potential endocrine disruptor. The compound's toxicity profile has been evaluated in regulatory studies, and appropriate safety measures should be followed when handling it. It is not intended for human consumption.

[1]. Weed management with CGA-362622, fluometuron, and prometryn in cotton. Weed Science, 50(5):642-647 (2002).

Prometryn is a colorless crystalline herbicide. It is a diamino-1,3,5-triazine compound with the chemical formula N,N'-di(propyl-2-yl)-1,3,5-triazine-2,4-diamine, with a methylthiodiacyl group substituted at the 6-position. It is both a herbicide and an exogenous substance and environmental pollutant. It is a diamino-1,3,5-triazine compound and also a methylthio-1,3,5-triazine compound. Prometryn is a selective herbicide that controls annual grasses and broadleaf weeds in a variety of crops, including cotton and celery. It works by inhibiting photosynthesis in sensitive plants. Prometryn is available in wettable powder and liquid formulations. Prometryn is a mildly to moderately toxic compound, classified as either Category II or Category III depending on the formulation. It is a triazine compound used as a selective pre- and post-emergence herbicide. (Excerpt from Merck Index, 11th Edition) Mechanism of Action…Their primary mode of action appears to be related to carbohydrate metabolism. Chlorotriazine compounds inhibit starch accumulation by blocking sugar production. Methoxy and methylthiotriazine compounds also exhibit similar effects. Triazine compounds have been reported to affect the tricarboxylic acid cycle, activating phosphophenylpyruvate carboxylase, leading to the consumption of sucrose and glyceric acid, and the production of aspartic acid and malic acid. /Triazine Compounds/
Inhibit the photolysis of water during photosynthesis. Furthermore, it also inhibits oxidative phosphorylation in plants.
In plants, its primary mechanism of action is the inhibition of photolysis of water during photosynthesis. Prometryn has also been shown to have other biological effects, such as inhibition of oxidative phosphorylation.
Mechanism of action in target species: inhibition of electron transport.
For more complete data on the mechanisms of action of Prometryn (7 compounds), please visit the HSDB record page.
Prometryn (CAS 7287-19-6) is a triazine herbicide used to control annual grasses and broadleaf weeds in crops such as cotton and celery. Its molecular formula is C₁₀H₁₉N₅S and its molecular weight is 241.36 g/mol. It is an inhibitor of photosynthesis. It is also used as an analytical reference standard. It is not approved for human therapeutic use.

C10H19N5S

241.3564

241.136

7287-19-6

Prometryn-d14;1202864-57-0

4929

Crystals
White powder
WHITE SOLID

1.2±0.1 g/cm3

322.8±25.0 °C at 760 mmHg

118-120°C

149.0±23.2 °C

0.0±0.7 mmHg at 25°C

1.602

1.91

2

6

5

16

182

0

S(C([H])([H])[H])C1=NC(=NC(=N1)N([H])C([H])(C([H])([H])[H])C([H])([H])[H])N([H])C([H])(C([H])([H])[H])C([H])([H])[H]

AAEVYOVXGOFMJO-UHFFFAOYSA-N

InChI=1S/C10H19N5S/c1-6(2)11-8-13-9(12-7(3)4)15-10(14-8)16-5/h6-7H,1-5H3,(H2,11,12,13,14,15)

6-methylsulfanyl-2-N,4-N-di(propan-2-yl)-1,3,5-triazine-2,4-diamine

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

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

DMSO : ~100 mg/mL (~414.32 mM)

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.)