The treatment Tebuconazole (TEB) (20–80 μM, 24 hours) leads HepG2 cells to accumulate nutrients [2]. In HepG2 cells, tebuconazole (20–80 μM, 12 hours) promotes peroxisome proliferation. Tebuconazole (20–80 μM, 24 hours) raises the HepG2 cells' mitochondrial membrane oxidation level. Protein is increased when bodily triglycerides are lost and oxidized. nutrients and oxidation-related markers' translocation and expression [2]. By activating the middle region of the ER, tebuconazole (0-750 μM, 24 levels) can impair MAC-T cell survival and proliferation and promote MAC-T cell inflammation [3]. Within H9c2 cells, tebuconazole (0 Tebuconazole (30–60 μM, 24 hours) can cause DNA damage and activity.

Tebuconazole (TEB) (10-50 mg/kg once daily for 28 days) induces multiple CYPs and EGFR, inhibits testicular P450 and glutathione S-transferase activity, reports Tebuconazole (25-100 mg/kg per day, continued for 10 days) causes fetal testicular Leydig cell proliferation during pregnancy and increases fetal testosterone and progesterone levels [6]. .Amoscanate (500 mg/kg; oral; 10 days) affects the ependyma and periventricular brain [1]. Amoscarate (250 and 500 mg/kg; oral; 28 days) induces medial striatal ependymal/subependymal localized necrosis, Ca++-positive microparticles, pyknosis, and edema [1]. Amoscarate (25 to 500 mg/kg; oral; 20 days) produces progressive ependymal necrosis [1]. Amoscanate induces severe ultrastructural damage to ependymal cells [1].

Western Blot analysis [2]
Cell Types: HepG2 cells
Tested Concentrations: 20, 40, 80 μM
Incubation Duration: 1– 12 hour
Experimental Results: Increased nuclear translocation of peroxisome proliferator-activated receptor. As well as expression of cluster of differentiation 36, fatty acid transport protein (FATP) 2, FATP5 and carnitine palmitoyltransferase 1.

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Apoptosis analysis [3 ]
Cell Types: Bovine Mammary Epithelial Cells (MAC-T cells)
Tested Concentrations: 100,150,200,250,500,750 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: Cell viability and proliferation are diminished and induced by pro-apoptotic proteins such as cleaved caspases 3 and 8 and Upregulation of BAX) activates apoptotic cell death. Induces loss of mitochondrial membrane potential in MAC-T cells. Induces mitochondria-mediated apoptosis of MAC-T cells by activating ER stress. Induces endoplasmic reticulum (ER) stress by upregulating Bip/GRP78 stim; PDI; ATF4; cleavage; and ERO1-Lα.

Animal/Disease Models: Male Wistar rat [5]
Doses: 10, 25 and 50 mg/kg
Route of Administration: Orally, one time/day for 28 days
Experimental Results: Induction of CYP1A1/2, CYP2B1/2, CYP2E1 and CYP3A proteins in the liver . The glutathione content in the liver is diminished, and the activities of glutathione S-transferase, superoxide dismutase, catalase and glutathione peroxidase are increased. Superoxide dismutase activity is increased in the kidneys and testicles. Glutathione S-transferase activity is diminished in the testicles. Serum testosterone concentration and cauda epididymal sperm count diminished.

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Animal/Disease Models: Male and female SD (SD (Sprague-Dawley)) rats [6]
Doses: 25, 50 and 100 mg/kg
Route of Administration: po (oral gavage) for 10 days
Experimental Results: Increased fetal serum testosterone and progesterone levels. Increases the number of fetal Leydig cells per testis without inducing cell aggregation. Upregulates the expression levels of Star, Cyp11a1, Hsd17b3 and Fshr. AKT1, ERK1/2, and mTOR phosphorylation were increased, BCL2 levels

Absorption, Distribution and Excretion
In animals, the drug was almost completely eliminated (>99%) after three days. Tebuconazole was excreted in urine and feces. (Phenyl-U-14C)-/tebuconazole/ (specific activity: 84.4 mCi/mg; radiochemical purity: >99%) was administered as a single dose of 2 or 20 mg/kg to five male and female rats per group, or as a single dose of 2 mg/kg of the labeled substance after 14 consecutive days of administration of the non-radiolabeled test substance. The levels of the radiolabeled substance in plasma, urine, and feces of all groups, as well as in bile and exhaled CO2 of each group, were determined. The maximum relative concentration in plasma ranged from 0.11 to 0.20 and was reached 0.33 to 1.7 hours after administration. Excretion rates were between 91% and 98% after 72 hours. Sex-related differences in excretion were observed, with a urine/fecal ratio of 16/78 in males and 30/62 in females. Bile excretion was measured only in males. Following a single liver pass, 90% of the radiolabeled substance was recovered in bile. Only 0.03% of the radiolabeled substance was recovered in exhaled air. After 72 hours, residual radiolabeled substance levels in tissues (excluding the gastrointestinal tract) ranged from 0.21% to 0.67% of the administered dose. (Phenylenol-U-14C)-/tebuconazole/ (specific activity: 84.4 mCi/mg; radiochemical purity: >99%) was administered as a single dose of 2 or 20 mg/kg to five male and female rats per group, or as a single dose of 2 mg/kg of the labeled substance after 14 consecutive days of administration of the unlabeled test substance. (Triazole-3,5-14C)-/tebuconazole/ (specific activity: 56.5 mCi/mg; radiochemical purity: 98.4%) was administered as a single dose of 20 mg/kg to five male and female rats in each group. Radiolabeled substances were detected in urine and feces of all groups over a period of up to 72 hours, and the chemical structures of specific radiolabeled metabolites were identified. Renal clearance was higher in female rats than in male rats (26%–35% vs. 15%–18%, respectively). Conversely, male rats excreted a higher proportion of radioactive material in feces (77%–80% vs. 60%–67%, respectively). Following oral administration of tebuconazole to rats, 65%–80% of the dose was cleared via bile and feces, while approximately 16%–35% was cleared in urine. Bile and fecal clearance was higher in male rats than in female rats. Biotransformation occurred primarily through oxidation, producing hydroxyl, carboxyl, triol, and keto acid metabolites and their conjugates, as well as triazoles. For more complete data on the absorption, distribution, and excretion of tebuconazole (6 types), please visit the HSDB record page. Metabolism/Metabolites Biotransformation occurs primarily through oxidation reactions, producing hydroxyl, carboxyl, triol, and keto acid metabolites and their conjugates, as well as triazoles. Among the identified metabolites, the oxidation of the pentane chain's 5 carbon to an alcohol, followed by further oxidation to a carboxyl group, is the main pathway. These metabolites are then further conjugated with sulfates or glucuronic acids. At high dose levels, the metabolic profile changes, with a higher proportion of alcohol metabolites compared to carboxyl-containing metabolites. Treatment with the labeled triazole moiety yields essentially the same results as with the unlabeled triazole moiety, except that the labeled triazole is recovered in the urine. ... In rats treated with tebuconazole labeled with ¹⁴C on either the benzene ring or the 3,5-triazole ring, regardless of prior treatment with the unlabeled compound, the main metabolites were oxidation products of the tert-butyl moiety methyl group, namely alcohols and carboxylic acids. In female animals, metabolism primarily produces simple oxidation products (e.g., hydroxyl and carboxyl metabolites), which then bind with glucuronic acid and sulfate, with only minor cleavage of the triazole moiety. In male animals, primary oxidation products are further oxidized to triol and keto acid derivatives; additionally, triazole cleavage occurs, consistent with results obtained using labeled triazole compounds. Free triazole constitutes approximately 5% of male urine and approximately 1.5% of female urine. The parent compound is present in small amounts. In a study of lactating goats, the metabolic pathway was similar to that of rats. The major metabolites identified were tert-butanol derivatives and their conjugates; the parent compound was also found. In a study of laying hens…, the hydroxylation of tert-butyl followed by sulfate conjugation was the major metabolic pathway.

Toxicity Data
LC50 (Rat) = 820 mg/m³/4h

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Non-human Toxicity Values LD50 (Rat, oral) >5000 mg/kg
LD50 (Mouse, oral) 1615 mg/kg
LD50 (Rabbit, oral) >1000 mg/kg
LD50 (Dog, oral) 625 mg/kg
For more complete non-human toxicity data for tebuconazole (7 items in total), please visit the HSDB records page.

[1]. Azole affinity of sterol 14α-demethylase (CYP51) enzymes from Candida albicans and Homo sapiens. Antimicrob Agents Chemother. 2013 Mar;57(3):1352-60.

[2]. Kwon HC, et.al. Tebuconazole Fungicide Induces Lipid Accumulation and Oxidative Stress in HepG2 Cells. Foods. 2021 Sep 22;10(10):2242.

[3]. Lee WY, et.al. Tebuconazole Induces ER-Stress-Mediated Cell Death in Bovine Mammary Epithelial Cell Lines. Toxics. 2023 Apr 21;11(4):397.

[4]. Ben Othmène Y,et.al. Tebuconazole induces ROS-dependent cardiac cell toxicity by activating DNA damage and mitochondrial apoptotic pathway. Ecotoxicol Environ Saf. 2020 Nov;204:111040.

[5]. Yang JD, et.al. Effects of tebuconazole on cytochrome P450 enzymes, oxidative stress, and endocrine disruption in male rats. Environ Toxicol. 2018 Jun 19.

[6]. Ma F, et.al. Gestational exposure to tebuconazole affects the development of rat fetal Leydig cells. Chemosphere. 2021 Jan;262:127792.

1-(4-chlorophenyl)-4,4-dimethyl-3-(1H-1,2,4-triazol-1-ylmethyl)pentane-3-ol is a tertiary alcohol in which the pentane-3-ol is substituted at positions 1, 4, 4, and 3 with 4-chlorophenyl, methyl, methyl, and 1H-1,2,4-triazol-1-ylmethyl, respectively. It belongs to the monochlorobenzene class, triazole class, and tertiary alcohol class.

C16H22CLN3O

307.8184

307.145

107534-96-3

Tebuconazole-d9;1246818-83-6

86102

White to off-white solid powder

1.1±0.1 g/cm3

476.9±55.0 °C at 760 mmHg

102-105°C

242.2±31.5 °C

0.0±1.3 mmHg at 25°C

1.564

3.58

1

3

6

21

326

0

PXMNMQRDXWABCY-UHFFFAOYSA-N

InChI=1S/C16H22ClN3O/c1-15(2,3)16(21,10-20-12-18-11-19-20)9-8-13-4-6-14(17)7-5-13/h4-7,11-12,21H,8-10H2,1-3H3

1-(4-chlorophenyl)-4,4-dimethyl-3-(1,2,4-triazol-1-ylmethyl)pentan-3-ol

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)

DMSO : ≥ 50 mg/mL (~162.43 mM)
H2O : ~0.1 mg/mL (~0.32 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (8.12 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (8.12 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (8.12 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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Solubility in Formulation 4: 20 mg/mL (64.97 mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)