Plant α-tubulin (α/β-tubulin heterodimer). Butralin binds specifically to plant α-tubulin, disrupting microtubule dynamics and inhibiting mitotic spindle formation. The compound also exhibits antimicrobial activity against Toxoplasma gondii and activates the human pregnane X receptor (PXR) signaling pathway with a potency of 39810.7 nM.

Butralin binds specifically to plant α-tubulin, halting cell division at prometaphase and disrupting the spatial orientation of cell wall deposition. It inhibits cell division of plant meristem, thus inhibiting the growth of weed buds and young roots, leading to weed death. The compound exhibits antimicrobial activity against Toxoplasma gondii RH infected in HFF cells.

In vivo, butralin is used as a dinitroaniline herbicide and plant growth regulator in flue-cured and air-dried tobacco. It inhibits cell division of plant meristem, leading to weed death. In animal studies, butralin generally exhibits low acute toxicity. The compound is used in agricultural research to study weed control mechanisms.

In vitro enzyme assays for butralin involve measuring its binding to tubulin and inhibition of microtubule polymerization. Plant tubulin is incubated with GTP and various concentrations of butralin. Microtubule polymerization is monitored spectrophotometrically by measuring the increase in absorbance at 340 nm. The compound's ability to inhibit microtubule assembly is assessed.

In vitro cellular assays for butralin involve treating plant cells or Toxoplasma gondii-infected cells with the compound and measuring cell division, growth, or viability. Plant cells are treated with various concentrations of butralin, and cell division is assessed by microscopy. Toxoplasma gondii viability is measured by plaque assay or metabolic activity.

In vivo animal studies for butralin are limited as the compound is primarily used as a herbicide. In animal studies, butralin generally exhibits low acute toxicity. The compound activates the human pregnane X receptor (PXR) signaling pathway. Further studies are needed to fully characterize its effects in animals.

Absorption, Distribution and Excretion
Extensively metabolized, primarily excreted in urine and feces. …Most (85%) of butril is excreted in urine within 48 hours (rat). After 72 hours, butril is undetectable in organs. In a metabolic study, rats were administered butril (ring-labeled) dissolved in corn oil by gavage at doses of 8 mg/kg/day (low dose) for single and multiple administrations, and 800 mg/kg/day (high-dose single administration) for a bile excretion study, and the distribution and excretion of butril were tracked over 7 days. Low-dose results showed that approximately 100% of the administered substance was excreted within approximately 2 days, with 55% to 60% excreted in feces and 35% to 45% in urine. Approximately 10% of unmetabolized butril was present in feces. The excretion half-life was approximately 12 hours. Only approximately 1% of the labeled butril remained in tissues. Similar excretion patterns were observed in repeated low-dose groups. Following high-dose bhutropine administration, it takes 5–7 days for 100% excretion of bhutropine in urine and feces. The excretion half-life is 2–4 days. In various tissues, fat and liver tend to retain more bhutropine residues. Females excrete bhutropine residues more slowly than males and retain more metabolites in tissues, particularly the liver and fat. Metabolism/Metabolites: In a bile excretion study using a low dose (8 mg bhutropine/kg), enterohepatic circulation was identified as the primary pathway for bhutropine excretion and metabolism. Twelve bhutropine metabolites were identified in mixed urine, feces, and/or bile samples. Metabolites at concentrations of 5% to 10% of the administered dose included: 2-methyl-5(6)[1-(1-carboxy-1-methyl)ethyl]-7(4)-nitrobenzimidazole, 2-methyl-5(6)[2-(1-hydroxy-2-methyl)propyl]-7(4)-nitrobenzimidazole, 2-methyl-2(4-amino-3,5-dinitrophenyl)propionic acid, and 2-methyl-2(4-amino-3,5-dinitrophenyl)propanol glucuronide. The concentration of the parent compound, buttraline, was 10% of the administered dose. No metabolites at concentrations higher than 10% of the administered dose were detected in this study. …In rats, buttraline is primarily metabolized through primary metabolic processes such as N-dealkylation, oxidation, and nitro reduction, and also through secondary metabolic processes such as N-acetyl conjugation and glucuronide conjugation. …Buttraline is ultimately metabolized to carbon dioxide.
Butralin has a molecular weight of 295.33 and a molecular formula of C14H21N3O4. It is a dinitroaniline herbicide. The compound is used as a plant growth regulator in tobacco. Further pharmacokinetic studies are needed to fully characterize its absorption, distribution, metabolism, and elimination in mammals.

Toxicity Data
LC50 (Rat) = 50,000 mg/m³/4h

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Preclinical toxicity studies of butralin have shown that it generally exhibits low acute toxicity in animals. The compound is a dinitroaniline herbicide that inhibits cell division by disrupting microtubule dynamics. It should be handled with appropriate safety precautions. Comprehensive toxicological evaluation is needed for any potential therapeutic applications.

Butralin is a C-nitro compound. Butralin is a dinitroaniline herbicide used as a plant growth regulator in flue-cured and air-dried tobacco. In animal studies, Butralin generally exhibits low acute toxicity. Oral exposure and eye irritation are classified as Group III, while dermal and inhalation exposure are classified as Group IV. The carcinogenicity classification of Butralin has not been determined.
Butralin is a dinitroaniline herbicide that inhibits cell division by disrupting microtubule dynamics and inhibiting mitotic spindle formation. It binds specifically to plant α-tubulin, halting cell division at prometaphase. Butralin is used as a plant growth regulator in tobacco. The compound exhibits low acute toxicity in animals and is used in agricultural research to study weed control mechanisms.

C14H21N3O4

295.34

295.153

33629-47-9

36565

Yellow orange crystals

1.2±0.1 g/cm3

381.3±42.0 °C at 760 mmHg

61ºC

184.4±27.9 °C

0.0±0.9 mmHg at 25°C

1.565

5.8

1

5

4

21

359

0

CCC(C)NC1=C(C=C(C=C1[N+](=O)[O-])C(C)(C)C)[N+](=O)[O-]

SPNQRCTZKIBOAX-UHFFFAOYSA-N

InChI=1S/C14H21N3O4/c1-6-9(2)15-13-11(16(18)19)7-10(14(3,4)5)8-12(13)17(20)21/h7-9,15H,6H2,1-5H3

N-butan-2-yl-4-tert-butyl-2,6-dinitroaniline

A 820; Tamex; Butralin

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 : ~100 mg/mL (~338.60 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (8.47 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 (8.47 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.)