Absorption, Distribution and Excretion
Atrazine (ATR) is a widely used chlorotriazine herbicide, a ubiquitous environmental contaminant, and a potential developmental toxicant. To quantitatively evaluate placental/lactational transfer and fetal/neonatal tissue dosimetry of ATR and its major metabolites, physiologically based pharmacokinetic models were developed for rat dams, fetuses and neonates. These models were calibrated using pharmacokinetic data from rat dams repeatedly exposed (oral gavage; 5mg/kg) to ATR followed by model evaluation against other available rat data. Model simulations corresponded well to the majority of available experimental data and suggest that: (1) the fetus is exposed to both ATR and its major metabolite didealkylatrazine (DACT) at levels similar to maternal plasma levels, (2) the neonate is exposed mostly to DACT at levels two-thirds lower than maternal plasma or fetal levels, while lactational exposure to ATR is minimal, and (3) gestational carryover of DACT greatly affects its neonatal dosimetry up until mid-lactation. To test the model's cross-species extrapolation capability, a pharmacokinetic study was conducted with pregnant C57BL/6 mice exposed (oral gavage; 5mg/kg) to ATR from gestational day 12 to 18. By using mouse-specific parameters, the model predictions fitted well with the measured data, including placental ATR/DACT levels. However, fetal concentrations of DACT were overestimated by the model (10-fold). This overestimation suggests that only around 10% of the DACT that reaches the fetus is tissue-bound. These rodent models could be used in fetal/neonatal tissue dosimetry predictions to help design/interpret early life toxicity/pharmacokinetic studies with ATR and as a foundation for scaling to humans.
... The atrazine (ATZ) concentrations in urine samples of the workers collected from an atrazine plant were determined by /a gas chromatograph-electron capture detector/ method /for detecting ATZ and its metabolites (deethylatrazine (DEA), deisopropylatrazine (DIA), deethyldeisopropylatrazine (DEDIA)) in human urine/. The concentration ranges were 0.003 -0.301 mg/L for DEDIA, 0.005 -0.011 mg/L for DEA, 0.006 -0.276 mg/L for DIA, and 0.005 -0.012 mg/L for ATZ.
Small amount of parent ... atrazine ... /was/ excreted in urine of cows fed unlabeled herbicide for 4 days.
Seventy-two hr /after ingestion/ 65.5% of radiolabeled atrazine was found in urine of rats, while 20.3% was found in the feces. Less than 0.1% was found in expired air, thus indicating s-triazine ring was not appreciably metabolized to carbon dioxide. Tissue analysis revealed that 15.8% of reactivity was retained, with high concentrations observed in the liver, kidney, and lung, and lower concentrations observed in muscle tissue and fat.
For more Absorption, Distribution and Excretion (Complete) data for Atrazine (7 total), please visit the HSDB record page.

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Metabolism / Metabolites
Atrazine (ATR) is a widely used chlorotriazine herbicide, a ubiquitous environmental contaminant, and a potential developmental toxicant. To quantitatively evaluate placental/lactational transfer and fetal/neonatal tissue dosimetry of ATR and its major metabolites, physiologically based pharmacokinetic models were developed for rat dams, fetuses and neonates. These models were calibrated using pharmacokinetic data from rat dams repeatedly exposed (oral gavage; 5mg/kg) to ATR followed by model evaluation against other available rat data. Model simulations corresponded well to the majority of available experimental data and suggest that: (1) the fetus is exposed to both ATR and its major metabolite didealkylatrazine (DACT) at levels similar to maternal plasma levels, (2) the neonate is exposed mostly to DACT at levels two-thirds lower than maternal plasma or fetal levels, while lactational exposure to ATR is minimal, and (3) gestational carryover of DACT greatly affects its neonatal dosimetry up until mid-lactation. To test the model's cross-species extrapolation capability, a pharmacokinetic study was conducted with pregnant C57BL/6 mice exposed (oral gavage; 5mg/kg) to ATR from gestational day 12 to 18. By using mouse-specific parameters, the model predictions fitted well with the measured data, including placental ATR/DACT levels. However, fetal concentrations of DACT were overestimated by the model (10-fold). This overestimation suggests that only around 10% of the DACT that reaches the fetus is tissue-bound. These rodent models could be used in fetal/neonatal tissue dosimetry predictions to help design/interpret early life toxicity/pharmacokinetic studies with ATR and as a foundation for scaling to humans.
Atrazine (ATR) is a widely used herbicide. There are several types of reactions in its metabolism. Herein, the mechanism of three paths of hydrolysis reactions in its metabolism and predictions of toxicities of its metabolites in the three paths will be presented. The calculation results by B3LYP (Becke, 3-parameter, Lee-Yang-Parr), one of the approaches in density functional theory, indicated that (1) there were three models in the three hydrolysis paths of ATR. The dissociation mechanisms of C(9/11)-N(8/10), C(4/6)-N(8/10), and C-Cl were dealkylation, deamination, and Cl substitution, respectively. (2) The energy barrier of C-Cl dissociation was lower. The dissociation was advantageous in dynamics and the primary reaction in the three hydrolysis paths. In these hydrolysis reactions, the different intermediates had different concentrations because of the impact of the reaction rate. (3) In addition, it was necessary to consider the solvent effect to investigate hydrolysis reaction. The conductor-like polarizable continuum model (CPCM) was used to simulate the hydrolysis reaction in bond length and energy barrier because of the solvent effect. Experimental or predictive results showed that atrazine and its metabolites in the three hydrolysis paths were carcinogenic.
Compounds of the s-triazine family are among the most heavily used herbicides over the last 30 years. Some of these derivatives are suspected to be carcinogens. In this study the identity of specific phase-I enzymes involved in the metabolism of s-triazine derivatives (atrazine, terbuthylazine, ametryne, and terbutryne) by human liver microsomes was determined. Kinetic studies demonstrated biphasic kinetics for all pathways examined (S-oxidation, N-dealkylation, and side-chain C-oxidation). Low Km values were in a range of about 1-20 uM, whereas high Km values were up to 2 orders of magnitude higher. For a correlation study, 30 human liver microsomal preparations were screened for seven specific P450 activities, and these were compared to activities for the metabolites derived from these s-triazines. A highly significant correlation in the high-affinity concentration range was seen with cytochrome P450 1A2 activities. Chemical inhibition was most effective with alpha-naphthoflavone an furafylline at low s-triazine concentrations and additionally with ketoconazole and gestodene at high substrate concentrations. Studies with 10 heterologously expressed P450 forms demonstrated that several P450 enzymes are capable of oxidizing these s-triazines, with different affinities and regioselectivities. P450 1A2 was confirmed to be the low-Km P450 enzyme involved in the metabolism of these s-triazines. A potential participation of flavin-containing monooxygenases (FMOs) in sulfoxidation reactions of the thiomethyl derivatives ametryne and terbutryne in human liver was also evaluated. Sulfoxide formation in human inhibition indicated no significant involvement of flavin-containing monooxygenases. Finally, purified recombinant FMO3, the major flavin-containing monooxygenase in human liver, exhibited no significant activity (< 0.1 nmol (nmol of FMO3)-1 min-1) in the formation of the parent sulfoxides of ametryne and terbutryne. Therefore, P450 1A2 alone is likely to be responsible for the hepatic oxidative phase-I metabolism of the s-triazine derivatives in exposed humans.
A large number of urinary metabolites was isolated and 15.8% was detected in the carcasses at 72 hr post-exposure. Dealkylation of atrazine in vitro, predominated over glutathione conjugation. Metabolites identified from rat and rabbit urine contained an intact triazine ring suggesting initial loss of ethyl or methyl groups from the alkyl side chains. In the miniature pig, atrazine and its metabolites were seen in urine for slightly more than 24 hr; diethylatrazine was also identified. Excretion by sheep and cattle is rapid with no residues seen in the milk of cows receiving 5 ppm atrazine in the diet for 4 days.
For more Metabolism/Metabolites (Complete) data for Atrazine (16 total), please visit the HSDB record page.

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Biological Half-Life
The whole body half-life of elimination /in rats/ was determined as 31.3 +/- 2.8 hours...

Toxicity Summary
IDENTIFICATION AND USE: Atrazine is a colorless powder. It is used for pre- and post-emergence control of annual broad-leaved weeds and annual grasses. It is also used in combinations with many other herbicides. HUMAN STUDIES: Potential symptoms of overexposure are irritation of eyes and skin, dermatitis, skin sensitization, dyspnea, weakness, incoordination, salivation, hypothermia, and liver injury. Two studies from northern Italy showed elevated risks of ovarian tumors among women exposed to triazine herbicides including atrazine. Small excess risks for cancer at a number of sites were associated with exposure either to unspecified triazine herbicides or specifically to atrazine. There was a positive association between atrazine exposure in drinking water and preterm birth. Atrazine failed to induce clastogenic and aneugenic damage in cultured human lymphocytes with metabolic activation. However, atrazine was found genotoxic in single-cell gel electrophoresis assay by using human peripheral blood lymphocytes with and without metabolic activation. Atrazine also induced unscheduled DNA synthesis in human EUE line cells. ANIMAL STUDIES: Atrazine is minimally irritating to skin and mildly irritating to eyes of rabbits. A 50% formulation was shown to be weakly irritating to the skin but did produce strong eye irritation including edema of the eyelid and conjuctivae of guinea pigs, rabbits, and cats. Cattle and sheep were killed by two daily doses of 250 mg/kg atrazine. Acutely poisoned sheep and cattle exhibited muscular spasms, fasciculations, stiff gait and increased respiratory rates. Adrenal degeneration and congestion of lung, liver and kidneys were observed. Rats fed diets that contained an equivalent of 10 or 50 mg/kg for 6 months showed growth retardation and slight leukopenia along with alterations of selective organ weights. Administration of atrazine by oral gavage at 100-600 mg/kg bw per day to rats for seven or 14 days induced both nephrotoxicity and hepatotoxicity. Atrazine disrupted the regular 4-day estrous cycles in rats. Short- and long-term studies performed with rats have shown that the mammary tumors induced in rats given high doses of atrazine in the diet are likely to be the result of an accelerating effect on normal, age-related perturbations of the estrous cycle, with resultant increase in exposure to endogenous estrogen and prolactin. The lack of effect of atrazine on the incidence of mammary tumors and other evidence of proliferative activity in ovariectomized rats fed the highest dose tested (400 ppm) suggests a non-genotoxic mechanism of action associated with hormonal imbalance. Atrazine was found to adversely affect the immune system in mice. Subcutaneous injection of atrazine at 800 mg/kg/day on days 3, 6, and 9 of gestation resulted in the death and resorption of some or all of the pups in each litter of rats. Dosages as high as 200 mg/kg by this route did not affect the number of pups per litter nor weight at weaning. Dietary levels up to 1000 ppm (about 50 mg/kg/day) also were harmless. Rats acutely treated with atrazine (100 mg/kg, bw) showed a significant decrease in spontaneous Purkinje cell firing rate. Atrazine also decreased the cerebellar potentials evoked by electrical stimulation of the ipsilateral radial nerve, affecting mostly the response to climbing fiber input. Neurobehavioral development of female and male mice daily exposed from Gestational Day 14 until Postnatal Day 21 to 1 or 100 ug/kg bw atrazine was investigated. Changes in exploratory profile and in affiliative/investigative behavior were observed, revealing a feminization of behavioral profile in atrazine-exposed males. Alteration in learning performance at adulthood was also evident. Atrazine alters steroidogenesis in male rats resulting in elevated serum corticosterone, progesterone, and estrogens. Atrazine is activated by plant enzymes to produce a mutagenic metabolite for Schizosaccharomyces pombe (forward mutation) and Chinese hamster cells (forward mutation). Atrazine is positive in the host mediated assay (mouse, yeast injected intrasanguineously) and induced chromosome aberrations in bone marrow cells of mice after single dose of 1 g/kg and 2 g/kg, respectively. ECOTOXICITY STUDIES: Weakness, tremors, ataxia, and weight loss occurred in mallards 1 hr after oral treatment with atrazine and persisted up to 11 days. In pheasants, remission had occurred by 5 days after treatment. In adult male Japanese quail, significantly longer comet tails of DNA damage in leukocytes and isolated hepatocytes were recorded with 500 mg/kg bw atrazine oral treatment. Atrazine did not mimic the effects of either estradiol or tamoxifen in male quail. Thus, atrazine did not exhibit overt estrogenic or anti-estrogenic activity. Conversely, atrazine augmented the effects of testosterone and estradiol on testis regression. It is concluded that atrazine up to 1000 ppm in the diet may exert some effects on reproductive development in sexually maturing male birds. Both endocrine and physiological effects of short-term, acute exposure to atrazine in juvenile barramundi (Lates calcarifer) was conducted in a controlled laboratory experiment. Expression of hepatic vitellogenin was not affected, supporting the notion that atrazine does not have a direct estrogenic effect via mediation of estrogen receptors. Atrazine exposure had profound influence on the oxidative stress markers and detoxifying enzyme of the exposed zebrafish. Sheepshead minnow embryo-juvenile exposure to atrazine found that a mean measured atrazine concentration of 3.4 mg/L had no effect on hatching success of embryos or growth of juveniles, but significantly reduced juvenile survival. The decrease in amphibian length and weight at metamorphosis may indicate a reduction in fitness in wild populations of anurans exposed to atrazine at 200 to 2,000 ug/L. Atrazine was found nontoxic to bees. Exposure and accumulation of atrazine caused oxidative toxicity and antioxidant response in maize.

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Interactions
...Arsenic uptake in grapes treated with MSMA /monosodium salt of methanearsonic acid/ and atrazine to control johnsongrass /was studied/. Arsenic residues five times higher than controls (0.24-0.28 ug/g dry weight) in grapes treated with MSMA and atrazine were found. ...It is evident that atrazine ...facilitates uptake of arsenic by plant.
HR96 is a CAR/PXR/VDR ortholog in invertebrates, and a promiscuous endo- and xenobiotic nuclear receptor involved in acclimation to toxicants. Daphnia HR96 is activated by chemicals such as atrazine and linoleic acid (LA) (n-6 fatty acid), and inhibited by triclosan and docosahexaenoic acid (DHA) (n-3 fatty acid). We hypothesized that inhibitors of HR96 may block the protective responses of HR96 based on previously performed luciferase assays. Therefore, we performed acute toxicity tests with two-chemical mixtures containing a HR96 inhibitor (DHA or triclosan) and a HR96 activator (LA or atrazine). Surprisingly, results demonstrate that triclosan and DHA are less toxic when co-treated with 20-80 uM atrazine. Atrazine provides concentration-dependent protection as lower concentrations have no effect and higher concentrations cause toxicity. LA, a weaker HR96 activator, did not provide protection from triclosan or DHA. Atrazine's protective effects are presumably due to its ability to activate HR96 or other toxicologically relevant transcription factors and induce protective enzymes. Atrazine did not significantly induce glucosyltransferase, a crucial enzyme in triclosan detoxification. However, atrazine did increase antioxidant activities, crucial pathways in triclosan's toxicity, as measured through GST activity and the TROLOX equivalence assay. The increase in antioxidant capacity is consistent with atrazine providing protection from a wide range of toxicants that induce ROS, including triclosan and unsaturated fatty acids predisposed to lipid peroxidation.
Atrazin is currently the most widely used herbicide in agriculture with lots of adverse effects on human health. Curcumin is a polyphenol known for its antioxidant, anti-inflammatory, and anticancer properties. In the present study, the protective effect of curcumin on atrazin-intoxicated rats is evaluated. Toxicity was induced by oral administration of atrazine (400 mg/kg/day) for 3 weeks. Curcumin at a dose of 400 mg/kg/day was given simultaneously by oral route. Redox status, mitochondrial function, 8-hydroxydeoxyguanosine (8-OHdG) level by immunoassay, and caspace-3 expression by immunohistochemistry were evaluated. Curcumin showed significant cardiac protection with improvement of redox status, mitochondrial function, 8-OHdG level, caspase-3 immunoreactivity, and cardiac muscle degeneration. From this current study, it can be concluded that administration of curcumin improved atrazine-induced cardiotoxicity through its modulatory effect on redox status, mitochondrial function, and caspase-3 expression.
Laboratory studies were conducted to determine the effects of different concentrations of fenhexamid and atrazine (25, 50 and 100 ug/L) on growth and oxidative stress on Scenedesmus obliquus (microalgae) after exposure for 24, 48, and 96 hr. In addition, residues of fenhexamid and atrazine were determined in the culture medium after 96 hr; 52%, 44% and 43% of fenhexamid remained in the medium for the lowest, middle and highest concentrations, respectively. Atrazine concentration decreased significantly in the medium with time. The reduction was faster with the lowest concentration (-53%), than in the highest concentration (-46%), while it was intermediate with 50 ug/L (-47%). The antioxidative enzyme activities were used as biomarkers to evaluate the toxic effects of fenhexamid and atrazine on the microalgae. Enzymatic activities were measured in the presence of each compound alone after 24, 48 and 96 hr and also in mixture after 24 hr exposure. The results showed that fenhexamid and atrazine induced antioxidative enzyme activities (GST, CAT and GR) at different concentrations. Catalase activities (CAT) in both pesticides treated-algae were significantly increased. Additionally, an increase in gulathione-S-transferase (GST) was observed in algae after 24, 48 and 96 hr of exposure to both fenhexamid and atrazine. Antioxidative enzymes in fenhexamid and atrazine mixture treatment showed an antagonistic interaction after 24 hr of exposure in algae.
For more Interactions (Complete) data for Atrazine (13 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LC50 Rat inhalation >5800 mg/cu m 4hr
LC50 Rat inhalation >710 mg/cu m 4hr
LD50 Rat dermal >3,100 mg/kg bw
LD50 Mouse oral 1750-3992 mg/kg bw
For more Non-Human Toxicity Values (Complete) data for Atrazine (16 total), please visit the HSDB record page.

Atrazine is an herbicide that does not occur naturally. Pure atrazine is an odorless, white powder that is not very volatile, reactive, or flammable and that will dissolve in water. Atrazine is used to kill weeds, primarily on farms, but has also been used on highway and railroad rights-of-way. The EPA now restricts how atrazine can be used and applied; only trained people are allowed to spray it.
Atrazine can cause developmental toxicity and female reproductive toxicity according to The Environmental Protection Agency (EPA).
Atrazine is a white crystalline solid. Melting point 173-175 °C. Sinks in water. A selective herbicide used for season-long weed control in a variety of crops.
Atrazine is a diamino-1,3,5-triazine that is 1,3,5-triazine-2,4-diamine substituted by a chloro group at position 6 while one of hydrogens of each amino group is replaced respectively by an ethyl and a propan-2-yl group. It has a role as a herbicide, an environmental contaminant and a xenobiotic. It is a chloro-1,3,5-triazine and a diamino-1,3,5-triazine. It is functionally related to a 6-chloro-1,3,5-triazine-2,4-diamine.
Atrazine is a selective triazine herbicide. Inhalation hazard is low and there are no apparent skin manifestations or other toxicity in humans. Acutely poisoned sheep and cattle may show muscular spasms, fasciculations, stiff gait, increased respiratory rates, adrenal degeneration, and congestion of the lungs, liver, and kidneys. (From The Merck Index, 11th ed)
Atrazine has been reported in Apis cerana with data available.
Atrazine is an organic compound consisting of an s-triazine-ring is a widely used herbicide. Its use is controversial due to widespread contamination in drinking water and its associations with birth defects and menstrual problems when consumed by humans at concentrations below government standards. Although it has been banned in the European Union, it is still one of the most widely used herbicides in the world . Atrazine is a suspected teratogen, causing demasculinization in male northern leopard frog even at low concentrations, and an estrogen disruptor. A 2010 study found that atrazine rendered 75 percent of male frogs sterile and turned one in 10 into females. A 2002 study found that exposure to atrazine caused male tadpoles to turn into hermaphrodites - frogs with both male and female sexual characteristics. But another study, requested by EPA and funded by Syngenta, was unable to reproduce these results. Atrazine was banned in the European Union (EU) in 2004 because of its persistent groundwater contamination. In the United States, however, atrazine is one of the most widely used herbicides, with 76 million pounds of it applied each year, in spite of the restriction that used to be imposed. Its endocrine disruptor effects, possible carcinogenic effect, and epidemiological connection to low sperm levels in men has led several researchers to call for banning it in the US.Rates of biodegradation are affected by atrazine's low solubility, thus surfactants may increase the degradation rate. Though the two alkyl moieties readily support growth of certain microorganisms, the atrazine ring is a poor energy source due to the oxidized state of ring carbon. In fact, the most common pathway for atrazine degradation involves the intermediate, cyanuric acid, in which carbon is fully oxidized, thus the ring is primarily a nitrogen source for aerobic microorganisms. Atrazine may be catabolized as a carbon and nitrogen source in reducing environments, and some aerobic atrazine degraders have been shown to use the compound for growth under anoxia in the presence of nitrate as an electron acceptor, a process referred to as a denitrification. When atrazine is used as a nitrogen source for bacterial growth, degradation may be regulated by the presence of alternative sources of nitrogen. In pure cultures of atrazine-degrading bacteria, as well as active soil communitites, atrazine ring nitrogen, but not carbon are assimilated into microbial biomass. Low concentrations of glucose can decrease the bioavailability, whereas higher concentrations promote the catabolism of atrazine. Tyrone Hayes, Department of Integrative Biology, University of California, notes that all of the studies that failed to conclude that atrazine caused hermaphroditism were plagued by poor experimental controls and were funded by Syngenta, one of the companies that produce the chemical. The U.S. Environmental Protection Agency (EPA) and its independent Scientific Advisory Panel (SAP) examined all available studies on this topic including Hayes' work and concluded that there are 'currently insufficient data' to determine if atrazine affects amphibian development. Hayes, formerly part of the SAP panel, resigned in 2000 to continue studies independently. The EPA and its SAP made recommendations concerning proper study design needed for further investigation into this issue. As required by the EPA, Syngenta conducted two experiments under Good Laboratory Practices (GLP) and inspection by the EPA and German regulatory authorities. The paper concluded 'These studies demonstrate that long-term exposure of larval X. laevis to atrazine at concentrations ranging from 0.01 to 100 microg/l does not affect growth, larval development, or sexual differentiation.' Another independent study in 2008 determined that 'the failure of recent studies to find that atrazine feminizes X. laevis calls into question the herbicide's role in that decline.' A report written in Environmental Science and Technology (May 15, 2008) cites the independent work of researchers in Japan, who were unable to replicate Hayes' work. 'The scientists found no hermaphrodite frogs; no increase in aromatase as measured by aromatase mRNA induction; and no increase in vitellogenin, another marker of feminization.'
A selective triazine herbicide. Inhalation hazard is low and there are no apparent skin manifestations or other toxicity in humans. Acutely poisoned sheep and cattle may show muscular spasms, fasciculations, stiff gait, increased respiratory rates, adrenal degeneration, and congestion of the lungs, liver, and kidneys. (From The Merck Index, 11th ed)
See also: Nystatin (annotation moved to).

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Mechanism of Action
Atrazine (ATZ) is probably the most widely used herbicide in the world. However there are still many controversies regarding its impacts on human health. Our investigations on the role of pesticides in liver dysfunctions have led us to detect an inhibition of FSP1 expression of 70% at 50 um and around 95% at 500 uM of ATZ (p<0.01). This gene encodes the protein S100a4 and is a clinical biomarker of epithelial-mesenchymal transition (EMT), a key step in the metastatic process. Here we investigated the possible effect of ATZ on cell migration and noticed that it prevents the EMT and motility of the HepG2 cells induced by the phorbol ester TPA. ATZ decreases Fak pathway activation but has no effect on the Erk1/2 pathway known to be involved in metastasis in this cell line. These results suggest that ATZ could be involved in cell homeostasis perturbation, potentially through a S100a4-dependant mechanism.

C8H14CLN5

215.6833

215.093

1912-24-9

Atrazine-15N;287476-17-9;Atrazine-13C3,15N3;Atrazine-d5;163165-75-1

2256

Colorless powder
Colorless or white, crystalline powder

1.3±0.1 g/cm3

279.7±23.0 °C at 760 mmHg

175°C

122.9±22.6 °C

0.0±0.6 mmHg at 25°C

1.605

1.53

2

5

4

14

166

0

ClC1=NC(=NC(=N1)N([H])C([H])(C([H])([H])[H])C([H])([H])[H])N([H])C([H])([H])C([H])([H])[H]

MXWJVTOOROXGIU-UHFFFAOYSA-N

InChI=1S/C8H14ClN5/c1-4-10-7-12-6(9)13-8(14-7)11-5(2)3/h5H,4H2,1-3H3,(H2,10,11,12,13,14)

6-chloro-4-N-ethyl-2-N-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, avoid exposure to moisture.

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

DMSO : ~83.33 mg/mL (~386.36 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (11.59 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.)