Absorption, Distribution and Excretion
They are efficiently absorbed from intestine, and presumably there is some absorption across the skin and lung. /Urea-, uracil- and triazine-based herbicides/
Absorbed through both foliage and roots. It appears to penetrate foliage rapidly, minimizing removal from foliage by rain. /It is/ translocated acropetally through xylem from roots and foliage, accumulating in apical meristems.
In mammals, following oral admin, 73-85% is eliminated in metabolized form in feces within 24 hr.

---

Metabolism / Metabolites
Terbutryn ... was metabolized by both rats and goats after a single oral dose by one or more of the following pathways: S-demethylation, conversion of thiomethyl into hydroxyl, N-de-ethylation, oxidation of the terminal carbon of the ethyl group to a carboxylic acid, oxidation of a terminal carbon of the t-butyl group to an alcohol or a carboxylic acid, or conjugation with glucuronic acid.
Carbon-labeled terbutryn was admin as single oral doses to rats and goats. Urine was collected at intervals up to 72 hr and then analyzed ... after isolation of glucuronides by chromatographic procedures. Five conjugates isolated and identified were: 2-amino-4-(t-butylamino)-6-(S-glucuronyl)-s-triazine; 2-(t-butylamino)-4-ethylamino-6-(S-glucuronyl)-s-triazine; 2-ethyl-amino-(2-methyl)glucuronylpropyl)amino-6-(S-methylthio)-s-triazine; 2-amino-4-(2-(1-glucuronyl-2-methylpropyl)amino)-6-methylthio-s-triazine; 2-ethylamino-4-(2-(2-methyl propan-1-olyl)amino)-6-(S-glucuronyl)-s-triazine.
After administration of terbutryne to rats, urinary metabolites observed ... included: 2-hydroxy terbutryne; 2-amino-4-hydroxy-6-t-butylamino-s-triazine; 2-amino-4-t-butylamino-6-mercapto-s-triazine; two S-glucuronides and two t-butyl-O-glucuronides. Other metabolites were formed by one or a combination of the following reactions: N-alkyl oxidation to alcohols or acids: S-demethylation; N-deethylation; and disulfide formation.
Microsomes prepared from livers from 30 to 70 year old patients undergoing liver resection were incubated with 6.3 to 1,000 uM atrazine, terbuthylazine, terbutryne, or ametryne , and the incubation mixtures were analyzed for metabolites. The compounds produced a variety of metabolites indicative of S-oxidation, N-dealkylation, and side chain C-oxidation. The metabolites were formed by processes showing biphasic kinetics, Michaelis constants for the first and second phases varying from 1.4 to 20 uM and from 54 to 530 uM, respectively. Atrazine, terbuthylazine, ametryne, or terbutryne at 25 uM was incubated with human liver microsomes containing substrates for cytochrome-P4501A2 (CYP1A2), cytochrome-P4502A6, cytochrome-P4502D6, cytochrome-P4502C9, cytochrome-P4502C19, cytochrome-P4502E1, or cytochrome-P4503A4 (CYP3A4) isozymes. Other microsomal preparations were incubated with 25 or 600 uM of the S-triazines in the presence or absence of alpha-naphthoflavone (aNF), furafylline, quinidine, sulfaphenazole, diethyl-dithiocarbamate, gestodene, or ketoconazole, inhibitors of various specific cytochrome-P450 (P450) isozymes, at concentrations 5 to 10 times greater than their inhibition constants. Microsomal preparations containing substrates for CYP1A2 and CYP3A4 showed the best correlation with the rates of metabolism of the S-triazines. Only aNF and furafylline, inhibitors of CYP1A2, inhibited metabolism of the S-triazines. A human liver microsomal preparation with demonstrated high levels of flavin containing monooxygenase (FMO) activity and purified recombinant human FMO-3 were incubated with ametryne and terbutryne. The extent of sulfoxidation of the two compounds was determined. No significant formation of sulfoxide metabolites was detected, indicating that the FMO system was not involved in the metabolism of S- triazines by human liver microsomes. The authors conclude that these results clearly identify CYP1A2 as the major phase-I P450 isozyme that is involved in the metabolism of S-triazines by human liver microsomes.
For more Metabolism/Metabolites (Complete) data for TERBUTRYNE (7 total), please visit the HSDB record page.
Terbutryn has known human metabolites that include Terbutrynsulfoxide, t-Butylhydroxy-terbutryn, and 2-Hydroxyethylterbutryn.

Toxicity Data
LC50 (rat) > 8,000 mg/m3/4h

---

Non-Human Toxicity Values
LD50 Rabbit dermal >2,000 mg/kg
LD50 Rat oral 2450-2500 mg/kg
LD50 Rat oral 2045 mg/kg
LC50 Rat inhalation >8 mg/L/4 hr /80% formulation/
For more Non-Human Toxicity Values (Complete) data for TERBUTRYNE (8 total), please visit the HSDB record page.

Environ Sci Technol. 2014;48(1):244-54.

Terbutryn is a methylthio-1,3,5-triazine that is 2-(methylsulfanyl)-1,3,5-triazine substituted by a tert-butylamino and an ethylamino group at positions 2 and 4 respectively. It has a role as a herbicide, a xenobiotic and an environmental contaminant. It is a methylthio-1,3,5-triazine and a diamino-1,3,5-triazine.

---

Mechanism of Action
... Their chief mode of action appears to involve carbohydrate metabolism. The chlorinated s-triazines inhibit starch accumulation by blocking the prodn of sugars. Similar behavior has been shown for the methoxy & methylthio-s-triazines. It has been reported that the s-triazines affect the tricarboxylic acid cycle with activation of phospho-phenyl pyruvate-carboxylase causing the disappearance of sucrose & glyceric acid with the formation of aspartic & malic acids. /S-triazines/
Inhibition of photosynthesis by disruption of light reactions and blockade of electron transport is the mechanism of action of the 1,3,5-triazine herbicides. /1,3,5-Triazines, from table/
The influence of some s-triazine herbicides on acid phosphatase and phosphodiesterase from corn (Zea mays) roots were investigated. Terbutryn stimulated both phosphatases, whereas prometryn stimulated only the phosphodiesterase. Atrazine desmetryn, prometon, and simazine inhibited acid phosphatase. No effect was exerted by ametryn. The enzyme assays and the kinetic parameters demonstrated that the interferences observed were due to an action on the synthesis of one or both enzymes rather than on the enzyme reactions. The types of the N-alkyl and the chlorine-subsitutuent groups in the structures of the s-triazines tested appear important in determing the degree of the interference.

C10H19N5S

241.35636

241.136

886-50-0

Terbutryn-d5;1219804-47-3

13450

WHITE, CRYSTALLINE
White powder

1.45

154-160°C

104-105°C

2 °C

1.55

2.381

2

6

5

16

206

0

N1C(NCC)=NC(NC(C)(C)C)=NC=1SC

IROINLKCQGIITA-UHFFFAOYSA-N

InChI=1S/C10H19N5S/c1-6-11-7-12-8(15-10(2,3)4)14-9(13-7)16-5/h6H2,1-5H3,(H2,11,12,13,14,15)

2-N-tert-butyl-4-N-ethyl-6-methylsulfanyl-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

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (10.36 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.

---

Solubility in Formulation 2: ≥ 2.5 mg/mL (10.36 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.

---

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