Absorption, Distribution and Excretion
Atrazine (ATR) is a widely used chlortriazine herbicide, a pervasive environmental pollutant, and a potential developmental toxicant. To quantitatively assess placental/lactational transport and fetal/neonatal tissue doses of ATR and its major metabolite, we established physiological-based pharmacokinetic models in rat mothers, fetuses, and newborns. These models were first calibrated using pharmacokinetic data from rat mothers repeatedly exposed to ATR (gavage administration; 5 mg/kg) and then evaluated against other available rat data. The model simulations showed good agreement with most existing experimental data and indicated that: (1) fetal exposure to concentrations of atrazine (ATR) and its major metabolite dialkylatrazine (DACT) was similar to maternal plasma concentrations; (2) newborns were primarily exposed to DACT at concentrations two-thirds lower than maternal plasma or fetal concentrations, while lactational exposure to ATR was extremely low; and (3) pregnancy residues of DACT significantly affected neonatal dose distribution until mid-lactation. To test the model's ability to extrapolate across species, we conducted pharmacokinetic studies in pregnant C57BL/6 mice, administering ATR (5 mg/kg) via gavage from day 12 to day 18 of gestation. Using mouse-specific parameters, the model's predictions agreed well with the experimental data, including ATR/DACT concentrations in the placenta. However, the model overestimated the concentration of DACT in the fetus (by a factor of 10). This overestimation suggests that only about 10% of the DACT reaching the fetus binds to tissues. These rodent models can be used for fetal/neonatal tissue dosing predictions to help design/interpret early life toxicity/pharmacokinetic studies (using ATR) and as a basis for extrapolation to humans. Atrazine (ATZ) concentrations in worker urine samples collected from the atrazine plant were determined using gas chromatography-electron capture detector (GC-EID). This method is used to detect ATZ and its metabolites (desethylatrazine (DEA), desisopropylatrazine (DIA), and desethyldesisopropylatrazine (DEDIA)) in human urine. The concentration ranges of DEDIA, DEA, DIA, and ATZ were 0.003–0.301 mg/L, 0.005–0.011 mg/L, 0.006–0.276 mg/L, and 0.005–0.012 mg/L, respectively. Small amounts of the parent compound atrazine were excreted in the urine of dairy cows fed unlabeled herbicides for 4 days. 72 hours after ingestion, 65.5% of the radiolabeled atrazine was detected in rat urine, and 20.3% in feces. The concentration detected in exhaled breath was less than 0.1%, indicating that the triazine ring was not significantly metabolized to carbon dioxide. Tissue analysis showed that 15.8% of the reactivity was retained, with higher concentrations in the liver, kidneys, and lungs, and lower concentrations in muscle tissue and fat. For more complete data on the absorption, distribution, and excretion of atrazine (7 compounds), please visit the HSDB records page.

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Metabolites/Metabolites
Atrazine (ATR) is a widely used chlortriazine herbicide, as well as a pervasive environmental pollutant and a potential developmental toxicant. To quantitatively assess placental/lactational transport and fetal/neonatal tissue doses of ATR and its major metabolites, we established physiological-based pharmacokinetic models in rat mothers, fetuses, and newborns. These models were calibrated using pharmacokinetic data from rat mothers repeatedly exposed to ATR (gavage; 5 mg/kg) and then evaluated against other available rat data. The model simulations showed good agreement with most existing experimental data and indicated that: (1) fetal exposure to concentrations of atrazine (ATR) and its major metabolite dialkylatrazine (DACT) was similar to maternal plasma concentrations; (2) newborns were primarily exposed to DACT at concentrations two-thirds lower than maternal plasma or fetal concentrations, while lactational exposure to ATR was extremely low; and (3) pregnancy residues of DACT significantly affected neonatal dose distribution until mid-lactation. To test the model's cross-species extrapolation ability, we conducted pharmacokinetic studies in pregnant C57BL/6 mice, administering ATR (5 mg/kg) via gavage from day 12 to day 18 of gestation. Using mouse-specific parameters, the model's predictions agreed well with experimental data, including ATR/DACT concentrations in the placenta. However, the model overestimated the concentration of DACT in the fetus (by a factor of 10). This overestimation suggests that only about 10% of the DACT reaching the fetus binds to tissues. These rodent models can be used to predict fetal/neonatal tissue doses to help design and interpret early life toxicity/pharmacokinetic studies and lay the foundation for generalizing findings to humans. Atrazine (ATR) is a widely used herbicide. Its metabolism involves multiple reactions. This article will describe the mechanisms of three hydrolytic pathways in its metabolism and predict the toxicity of metabolites in these three pathways. The results of B3LYP (Becke three-parameter Lee-Yang-Parr) calculations using density functional theory methods show that: (1) There are three models for the three hydrolysis pathways of ATR. The dissociation mechanisms of C(9/11)-N(8/10), C(4/6)-N(8/10) and C-Cl bonds are dealkylation, deamination and Cl substitution, respectively. (2) The energy barrier for C-Cl bond dissociation is low. This dissociation is kinetically advantageous and is the main reaction in the three hydrolysis pathways. In these hydrolysis reactions, the concentrations of different intermediates vary due to the influence of the reaction rate. (3) In addition, the solvent effect needs to be considered when studying the hydrolysis reaction. Due to the solvent effect, the bond length and energy barrier of the hydrolysis reaction were simulated using a conductor-like polarized continuum model (CPCM). Experimental or predictive results show that atrazine and its metabolites in the three hydrolysis pathways are carcinogenic. Triazine compounds are among the most widely used herbicides in the past 30 years. Some of these derivatives are suspected of being carcinogenic. This study identified specific phase I enzymes involved in the metabolism of triazine derivatives (atrazine, terbutaline, atrazine, and terbutyne) in human liver microsomes. Kinetic studies showed that all detected metabolic pathways (S-oxidation, N-dealkylation, and side-chain C-oxidation) exhibited biphasic kinetics. Low Km values ranged from approximately 1–20 μM, while high Km values were two orders of magnitude higher. For correlation studies, we screened the activities of seven specific P450 enzymes in 30 human liver microsomal samples and compared them with the metabolic activities of these triazine derivatives. The results showed that, within the high affinity concentration range, the activity of cytochrome P450 1A2 was highly significantly correlated with the activity of the metabolites. Under low concentrations of S-triazine compounds, α-naphthylflavonoids and furazolidone showed the best chemoinhibitory effects; under high substrate concentrations, ketoconazole and pregnadienone also exhibited some inhibitory effects. Studies of 10 heterologously expressed P450 enzymes showed that multiple P450 enzymes could oxidize these s-triazine compounds, but with varying affinities and regioselectivities. P450 1A2 was identified as a low-Km P450 enzyme involved in the metabolism of these s-triazine compounds. Furthermore, the potential role of flavin monooxygenases (FMOs) in the sulfonation of the thiomethyl derivatives amitriptyline and tert-butyne in human liver was evaluated. Sulfonate generation in human liver inhibition assays indicated that flavin monooxygenases were not significantly involved in this reaction. Finally, purified recombinant FMO3 (the major flavin monooxygenase in human liver) showed no significant activity in the generation of sulfonates from the amatoxins and tert-butyne parent compounds (< 0.1 nmol (nmol FMO3)⁻¹ min⁻¹). Therefore, P450 1A2 is likely the only enzyme involved in the phase I metabolism of s-triazine derivative oxidation in the liver of exposed individuals. A large number of urinary metabolites were isolated, and 15.8% of the metabolites were detected in cadavers 72 hours after exposure. In vitro, atrazine dealkylation was stronger than glutathione conjugation. Metabolites identified from rat and rabbit urine contained intact triazine rings, indicating the initial loss of an ethyl or methyl group from the alkyl side chain. In miniature pigs, atrazine and its metabolites were detected in urine slightly beyond 24 hours; diethyl atrazine was also identified. Excretion was rapid in sheep and cattle; no residues were detected in milk from cows fed 5 ppm atrazine for 4 days. For more complete metabolite/metabolite data on atrazine (16 metabolites in total), please visit the HSDB record page.

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Biological Half-Life
The systemic elimination half-life measured in rats was 31.3 ± 2.8 hours…

Toxicity Summary
Identification and Uses: Atrazine is a colorless powder. It is used for pre- and post-emergence control of annual broadleaf and grass weeds. It is also often mixed with a variety of other herbicides. Human Studies: Potential symptoms of overexposure include eye and skin irritation, dermatitis, skin allergies, difficulty breathing, weakness, ataxia, salivation, hypothermia, and liver damage. Two studies in northern Italy have shown an increased risk of ovarian tumors in women exposed to triazine herbicides, including atrazine. Exposure to unspecified triazine herbicides or specifically to atrazine has been associated with a slight increased risk of cancers in multiple sites. Atrazine exposure in drinking water has been positively correlated with preterm birth. Atrazine failed to induce chromosome breakage and aneuploidy in metabolically activated cultured human lymphocytes. However, single-cell gel electrophoresis using metabolically activated and unactivated human peripheral blood lymphocytes revealed that atrazine is genotoxic. Atrazine can also induce unplanned DNA synthesis in human EUE cell lines. Animal studies: Atrazine has very low skin irritation in rabbits and mild eye irritation. 50% atrazine formulations have weak skin irritation but strong eye irritation in guinea pigs, rabbits, and cats, including eyelid and conjunctival edema. Cattle and sheep died after twice-daily injections of 250 mg/kg atrazine. Acutely poisoned cattle and sheep exhibited muscle spasms, fasciculations, gait stiffness, and increased respiratory rate. Adrenal degeneration and congestion of the lungs, liver, and kidneys were observed. Rats fed diets containing the equivalent of 10 or 50 mg/kg atrazine for 6 months showed growth retardation, mild leukopenia, and changes in the weight of some organs. Gavage administration of 100-600 mg/kg body weight/day of atrazine to rats for 7 or 14 days induced nephrotoxicity and hepatotoxicity. Atrazine disrupts the normal 4-day estrous cycle in rats. Short-term and long-term studies in rats have shown that high-dose atrazine-induced mammary tumors may be due to atrazine's acceleration of normal, age-related estrous cycle disruption, leading to increased exposure to endogenous estrogen and prolactin. In ovariectomized rats treated with the highest dose (400 ppm) of atrazine, atrazine had no effect on mammary tumor incidence or other proliferative activity markers, suggesting that its mechanism of action is not genotoxic but related to hormonal imbalance. Studies have found that atrazine has adverse effects on the immune system in mice. Subcutaneous injection of atrazine at a dose of 800 mg/kg/day on days 3, 6, and 9 of gestation resulted in partial or complete death or absorption of pups in each litter. Administration of doses up to 200 mg/kg via this route had no effect on litter size or weaning weight. Dietary atrazine levels up to 1000 ppm (approximately 50 mg/kg/day) were also harmless. In rats acutely administered atrazine (100 mg/kg body weight), the spontaneous firing rate of Purkinje cells was significantly reduced. Atrazine also reduced brain potentials induced by ipsilateral radial nerve electrical stimulation, primarily affecting responses to climbing fiber input. This study investigated the neurobehavioral development of male and female mice exposed daily to atrazine at 1 or 100 μg/kg body weight from day 14 of gestation to day 21 postnatal. Results showed altered exploratory and affinity/investigation behaviors in the mice, with atrazine-exposed male mice exhibiting feminized behavioral characteristics. Learning abilities in adult mice were also altered. Atrazine altered steroid production in male rats, leading to elevated serum corticosterone, progesterone, and estrogen levels. Upon activation by plant enzymes, atrazine produces a mutagenic metabolite in fissile yeast (positive mutant) and Chinese hamster cells (positive mutant). In host-mediated experiments (mice, intraserine injection with yeast), atrazine showed a positive response, inducing chromosomal aberrations in mouse bone marrow cells after single administration of 1 g/kg and 2 g/kg, respectively. Ecotoxicity studies: Mallards showed weakness, tremors, ataxia, and weight loss one hour after oral administration of atrazine, with symptoms lasting up to 11 days. Pheasants showed symptom relief five days after administration. In adult male Japanese quail, oral administration of 500 mg/kg body weight of atrazine significantly prolonged comet tails of DNA damage in leukocytes and isolated hepatocytes. Atrazine did not exhibit the effects of estradiol or tamoxifen in male quail. Therefore, atrazine does not possess significant estrogenic or anti-estrogenic activity. Conversely, atrazine enhanced the effects of testosterone and estradiol on testicular degeneration. It is concluded that at feed concentrations of up to 1000 ppm of atrazine may have some impact on the reproductive development of sexually mature male birds. In controlled laboratory experiments, the endocrine and physiological effects of short-term acute exposure to atrazine on juvenile Lates calcarifer were investigated. Hepatic vitellogenin expression was unaffected, supporting the view that atrazine does not produce a direct estrogenic effect mediated by estrogen receptors. Atrazine exposure significantly affected oxidative stress markers and detoxification enzymes in zebrafish. Atrazine exposure experiments on sheephead tadpole embryos to juveniles showed that an average concentration of 3.4 mg/L atrazine had no effect on embryo hatching rate or juvenile growth, but significantly reduced juvenile survival. Decreased body length and weight during amphibian metamorphosis may indicate reduced fitness in wild tailless amphibian populations exposed to atrazine concentrations ranging from 200 to 2000 μg/L. Atrazine was found to be non-toxic to bees. Exposure to and accumulation of atrazine led to oxidative toxicity and antioxidant responses in maize.
Interactions
...This study investigated the arsenic uptake in grapes when treated with MSMA (atrazine monosodium salt) and atrazine to control Johnson's grass. The results showed that the arsenic residues in grapes treated with MSMA and atrazine were five times higher than in the control group (0.24–0.28 μg/g dry weight). Clearly, atrazine promotes arsenic uptake in plants.
HR96 is a CAR/PXR/VDR homolog in invertebrates, a nuclear receptor with broad endogenous and exogenous activity involved in adaptation to toxins. In Daphnia davidii, HR96 can be 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). Based on previous luciferase activity assays, we hypothesized that HR96 inhibitors might block the protective response of HR96. Therefore, we conducted acute toxicity tests using a two-chemical mixture containing an HR96 inhibitor (DHA or triclosan) and an HR96 activator (LA or atrazine). Unexpectedly, the results showed that co-treatment with 20–80 μM atrazine reduced the toxicity of both triclosan and DHA. The protective effect of atrazine was concentration-dependent; low concentrations were ineffective, while high concentrations led to toxicity. LA (a weaker HR96 activator) provided no protection against either triclosan or DHA. The protective effect of atrazine may stem from its ability to activate HR96 or other toxicology-related transcription factors and induce protective enzymes. Atrazine did not significantly induce the expression of glucosyltransferase (an enzyme that plays a key role in triclosan detoxification). However, atrazine did enhance antioxidant activity, a key pathway in triclosan toxicity, as confirmed by GST activity and TROLOX equivalence assays. The enhanced antioxidant capacity is consistent with atrazine's ability to protect the body from various reactive oxygen species (ROS) toxins, including triclosan and unsaturated fatty acids prone to lipid peroxidation. Atrazine is currently the most widely used herbicide in agriculture and has many adverse effects on human health. Curcumin is a polyphenol compound known for its antioxidant, anti-inflammatory, and anticancer properties. This study evaluated the protective effect of curcumin against atrazine poisoning in rats. Rats were induced to poison by oral administration of atrazine (400 mg/kg/day) for 3 weeks. Simultaneously, curcumin was administered orally at a dose of 400 mg/kg/day. Redox status, mitochondrial function, 8-hydroxydeoxyguanosine (8-OHdG) levels were assessed by immunoassay, and caspase-3 expression was assessed by immunohistochemistry. The results showed that curcumin significantly improved redox status, mitochondrial function, 8-OHdG levels, caspase-3 immunoreactivity, and myocardial degeneration, thereby significantly protecting the heart. This study demonstrates that curcumin can mitigate atrazine-induced cardiotoxicity by regulating redox state, mitochondrial function, and caspase-3 expression. Laboratory studies were conducted to determine the effects of different concentrations of benzoylcarbamate and atrazine (25, 50, and 100 μg/L) on the growth and oxidative stress of Scenedesmus obliquus (a microalga), after exposure for 24, 48, and 96 hours. Furthermore, the residual amounts of benzoylcarbamate and atrazine in the culture medium were measured after 96 hours; the residual amounts of benzoylcarbamate in the lowest, medium, and highest concentration groups were 52%, 44%, and 43%, respectively. The concentration of atrazine in the culture medium decreased significantly over time. The fastest decrease was observed at the lowest concentration (-53%), followed by the highest concentration (-46%), while the decrease at a concentration of 50 μg/L was intermediate (-47%). Antioxidant enzyme activity was used as a biomarker to assess the toxic effects of benzoylcarbamide and atrazine on microalgae. Enzyme activities were determined after treatment with each compound alone for 24, 48, and 96 hours, and after treatment with a mixture of both compounds for 24 hours. Results showed that both benzoylcarbamide and atrazine induced the activity of antioxidant enzymes (glutathione S-transferase, catalase, and glutathione reductase) at different concentrations. Catalase (CAT) activity was significantly increased in algae treated with both pesticides. Furthermore, glutathione S-transferase (GST) activity was also significantly increased in algae after exposure to benzoylcarbamide and atrazine for 24, 48, and 96 hours. In algae, antioxidant enzymes showed antagonistic effects after 24 hours of treatment with the mixture of benzoylcarbamide and atrazine. More complete data on atrazine interactions (13 items in total) can be found on the HSDB record page.

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Non-human toxicity values
Rat inhalation LC50 >5800 mg/m³ 4 hours
Rat inhalation LC50 >710 mg/m³ 4 hours
Rat dermal LD50 >3100 mg/kg body weight
Mouse oral LD50 1750-3992 mg/kg body weight
For more complete (16) non-human toxicity values of atrazine, please visit the HSDB record page.

Atrazine is a herbicide that does not exist naturally. Pure atrazine is an odorless white powder with low volatility, reactivity, and flammability, and is readily soluble in water. Atrazine is primarily used for weed control, especially on farms, but has also been used along highways and railways. The U.S. Environmental Protection Agency (EPA) currently imposes strict restrictions on the use and application of atrazine; only trained personnel are permitted to spray it. According to the EPA, atrazine may cause developmental toxicity and female reproductive toxicity. Atrazine is a white crystalline solid with a melting point of 173-175°C and sinks in water. Atrazine is a selective herbicide that can be used for weed control on a variety of crops throughout the growing season. Atrazine is a diamino-1,3,5-triazine compound with the structure 1,3,5-triazine-2,4-diamine, with a chlorine substitution at the 6-position and a hydrogen atom on each amino group replaced by an ethyl or a propionic-2-yl group, respectively. It is both a herbicide and an environmental pollutant and exogenous substance. It is a chloro-1,3,5-triazine compound and also a diamino-1,3,5-triazine compound. Its structure is similar to 6-chloro-1,3,5-triazine-2,4-diamine. Atrazine is a selective triazine herbicide. It has low inhalation hazard and no obvious skin reactions or other toxicities in humans. Acute poisoning in sheep and cattle may cause muscle spasms, fasciculations, stiff gait, increased respiratory rate, adrenal insufficiency, and congestion of the lungs, liver, and kidneys. (Excerpt from Merck Index, 11th edition) Atrazine has been reported to exist in the Chinese honeybee (Apis cerana), and there is relevant data. Atrazine is an organic compound composed of an S-triazine ring and is a widely used herbicide. Atrazine's use is controversial due to widespread contamination of drinking water and its potential to cause birth defects and menstrual problems even at concentrations below government standards. Despite being banned in the EU, atrazine remains one of the most widely used herbicides in the world. It is suspected of being teratogenic, causing demasculinization in male northern leopard frogs even at low concentrations, and is an estrogen disruptor. A 2010 study found that atrazine caused 75% of male frogs to become infertile and one in ten to become female. A 2002 study found that atrazine exposure caused male tadpoles to become hermaphroditic—frogs exhibiting both male and female sexual characteristics. However, another study commissioned by the US Environmental Protection Agency and funded by Syngenta failed to replicate these results. The EU banned atrazine in 2004 due to its continued groundwater contamination. However, in the US, despite past restrictions, atrazine remains one of the most widely used herbicides, with annual usage reaching 76 million pounds. Its endocrine-disrupting effects, potential carcinogenicity, and epidemiological link to reduced sperm count in men have prompted some researchers to call for a ban on atrazine in the United States. The biodegradation rate of atrazine is affected by its low solubility, so surfactants may help improve its degradation rate. Although the two alkyl moieties can promote the growth of some microorganisms, the atrazine ring has a poor energy source due to the oxidized state of the ring carbon. In fact, the most common degradation pathway of atrazine involves the intermediate cyanuric acid, where the carbon is completely oxidized, thus the ring primarily serves as a nitrogen source for aerobic microorganisms. In reducing environments, atrazine can be metabolized as both a carbon and nitrogen source, and some aerobic atrazine-degrading bacteria have been shown to utilize this compound for growth under anaerobic conditions, using nitrate as an electron acceptor—a process known as denitrification. When atrazine is used as a nitrogen source for bacterial growth, its degradation may be regulated by other nitrogen sources. In pure cultures of atrazine-degrading bacteria and in active soil microbial communities, the nitrogen (not carbon) on the atrazine ring is absorbed by the microbial biomass. Low concentrations of glucose reduce the bioavailability of atrazine, while high concentrations promote its catabolism. Tyrone Hayes of the Department of Integrative Biology at the University of California points out that all studies that failed to conclude that atrazine causes hermaphroditism suffered from poor experimental controls, and these studies were funded by Syngenta, one of the companies that produces the chemical. The U.S. Environmental Protection Agency (EPA) and its independent Scientific Advisory Panel (SAP) reviewed all existing research on the subject, including Hayes's study, and concluded that there was currently "insufficient data" to determine whether atrazine affects amphibian development. Hayes, a former member of the SAP panel, resigned in 2000 to continue his independent research. The EPA and SAP made recommendations on appropriate research designs needed for further investigation into this issue. At the EPA's request, Syngenta conducted two experiments under Good Laboratory Practice (GLP) guidelines and underwent inspections by the EPA and German regulatory agencies. The paper concludes: "These studies show that long-term exposure of Xenopus larvae to atrazine at concentrations of 0.01 to 100 μg/L does not affect their growth, larval development, or sexual differentiation." Another independent study in 2008 noted, "Recent studies have failed to find that atrazine causes feminization in Xenopus larvae, raising questions about the role of this herbicide in the decline of Xenopus populations." A report in Environmental Science & Technology (May 15, 2008) cited independent research by Japanese researchers who were unable to replicate Hayes's findings. "Scientists did not find hermaphroditic frogs; did not find an increase in aromatase mRNA-induced aromatase levels; and did not find an increase in vitellogenin (another marker of feminization)." A selective triazine herbicide. Low inhalation hazard, with no obvious skin manifestations or other toxicities in humans. Acute poisoning in sheep and cattle may cause muscle spasms, fasciculations, stiff gait, increased respiratory rate, adrenal degeneration, and congestion of the lungs, liver, and kidneys. (Excerpted from Merck Index, 11th edition)
See also: Nystatin (note moved to).

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Mechanism of Action
Atrazine (ATZ) is perhaps the most widely used herbicide in the world. However, its effects on human health remain highly controversial. Our study on the role of pesticides in liver dysfunction showed that at a concentration of 50 μM ATZ, FSP1 expression was inhibited by 70%, while at a concentration of 500 μM ATZ, the inhibition rate was approximately 95% (p<0.01). This gene encodes the S100a4 protein, a clinical biomarker of epithelial-mesenchymal transition (EMT), a key step in the metastasis process. This study investigated the potential effects of ATZ on cell migration and found that ATZ inhibited phorbol ester (TPA)-induced EMT and migration ability in HepG2 cells. ATZ reduced the activation of the Fak signaling pathway but had no effect on the Erk1/2 signaling pathway, which is known to be involved in the metastasis of this cell line. These results suggest that ATZ may participate in the disruption of cellular homeostasis through an S100a4-dependent 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.)