Absorption, Distribution and Excretion
IN CHRONIC TOXICITY STUDIES ... LINURON ... CONTINUOUSLY FED TO RATS & DOGS FOR ... TWO YR AT DIETARY LEVELS ... FROM 25 TO 2500 PPM ... TOTAL ANILINE-CONTAINING RESIDUES IN BLOOD & ... (MUSCLE, FAT, LIVER, KIDNEY, SPLEEN) WERE A FEW TO 100 PPM. ... RESIDUES REPRESENTED ONLY MINUTE FRACTION OF ... HERBICIDE INGESTED BY ANIMALS.
LINURON IS MOST READILY ABSORBED THROUGH THE ROOT SYSTEM; LESS SO THROUGH FOLIAGE & STEMS. HOWEVER, FOLIAR ABSORPTION ... IS SIGNIFICANTLY GREATER THAN THAT OF DIURON, MONURON, OR FENURON. ... TRANSLOCATION IS PRIMARILY UPWARD IN THE XYLEM.
... RESIDUE DATA ... OBTAINED IN SHORT TERM ELIMINATION EXPERIMENTS ... . AMT OFRADIOACTIVITY WHICH PERSISTED IN BLOOD & DIFFERENT TISSUES AT END OF 72 HR ... PERIODS WERE NO MORE & USUALLY MUCH LESS THAN 1% OF DOSE APPLIED.

---

Metabolism / Metabolites
... LINURON-INDUCIBLE ENZYME WAS OBTAINED FROM BACILLUS SPHAERICUS. THIS ACYLAMIDASE DEGRADED LINURON BY HYDROLYSIS OF AMIDE BOND WITH ... RELEASE OF CARBON DIOXIDE & N,O-DIMETHYL HYDROXYLAMINE. ... ENZYME WAS SPECIFIC FOR METHOXY-SUBSTITUTED PHENYLUREAS & DID NOT HYDROLYZE 1,1-DIMETHYL PHENYLUREAS ... .
IN GREENHOUSE STUDIES, LINURON ENTERED CORN (ZEA MAYS L), SOYBEAN (GLYCINE MAX L) & CRABGRASS (DIGITARIA SANGUINALIS L) WITH ABSORBED WATER. DEMETHYL LINURON & 3,4-DICHLORO-ANILINE WERE FOUND IN TISSUES. ... SOME LINURON BOUND WITHIN PLANT ... .
LINURON ... FED TO ALBINO RATS. URINE ... ANALYZED FOR METABOLITES /&/ N-(3,4-DICHLOROPHENYL)UREA, N-(3,4-DICHLOROPHENYL)-N'-METHYLUREA & 3,4-DICHLOROANILINE WERE FOUND FREE. N-(2-HYDROXY-4,5-DICHLOROPHENYL)-N'-METHYLUREA, N-(5-HYDROXY-3,4-DICHLOROPHENYL)UREA & 6-ACETAMIDO-2,3-DICHLOROPHENOL ... /WERE IDENTIFIED/ AS GLUCURONIDES OR SULFATES.
In rats linuron is metabolized by demethoxylation followed by hydroxylation of the benzene ring. Major urinary metabolites are urea derivatives; no unchanged linuron could be demonstrated. Only trace amounts of 3,4-dichloroaniline were found. If metabolism to dichloroaniline is major pathway in humans, ... methemoglobinemia should be anticipated after toxic doses.
For more Metabolism/Metabolites (Complete) data for LINURON (9 total), please visit the HSDB record page.

Toxicity Summary
Linuron is a weak competitive inhibitor of androgen receptor binding and it inhibits androgen-induced gene expression in vitro. This may partially contribute to the malformations of androgen-dependent tissues in male rats. (A9961)

---

Toxicity Data
LC50 (rat) = 48 mg/m3/4h

---

Non-Human Toxicity Values
LD50 Rabbit percutaneous greater than 5000 mg ai (as 50% wettable powder)/kg
LD50 Rat female oral 4000 mg/kg in starch mucilage /Technical linuron/
LC50 Rat inhalation >4.06 mg/l air/4 hr
LD50 Rabbit oral 2250 mg/kg
For more Non-Human Toxicity Values (Complete) data for LINURON (11 total), please visit the HSDB record page.

[1]. Functional Redundancy of Linuron Degradation in Microbial Communities in Agricultural Soil and Biopurification Systems. Appl Environ Microbiol. 2016 Apr 18;82(9):2843-2853.

[2]. Cellular and Molecular Mechanisms of Action of Linuron: An Antiandrogenic Herbicide That Produces Reproductive Malformations in Male Rats. Toxicol Sci. 2000 Aug;56(2):389-99.

[3]. Reproductive Toxicity of Linuron Following Gestational Exposure in Rats and Underlying Mechanisms. Toxicol Lett. 2017 Jan 15;266:49-55.

[4]. Various Effects of the Photosystem II--inhibiting Herbicides on 5-n-alkylresorcinol Accumulation in Rye Seedlings. Pestic Biochem Physiol. 2014 Nov;116:56-62.

Linuron can cause developmental toxicity according to The Environmental Protection Agency (EPA).
Linuron appears as colorless crystals. Non corrosive. Used as an herbicide.
Linuron is a member of the class of phenylureas that is N-methyl urea substituted by a methoxy group at position 1 and a 3,4-dichlorophenyl group at position 3. It has a role as a xenobiotic, an environmental contaminant, a herbicide and an agrochemical. It is a dichlorobenzene and a member of phenylureas. It is functionally related to a N-methyl urea.
Linuron is an herbicide for the pre- and post-emergence control of annual grass and broad-leaved weeds using selective and systemic action with contact and residual action. It is known to inhibit photosynthesis (photosystem II).
A selective pre- and post-emergence herbicide. (From Merck Index, 11th ed)

---

Mechanism of Action
Inhibits photosynthesis.

C9H10CL2N2O2

249.09

248.011

330-55-2

Linuron-d6;1219804-76-8

9502

White to off-white solid powder

1.3±0.1 g/cm3

361.7±52.0 °C at 760 mmHg

93-94°C

172.6±30.7 °C

0.0±0.9 mmHg at 25°C

1.556

3.33

1

2

2

15

228

0

XKJMBINCVNINCA-UHFFFAOYSA-N

InChI=1S/C9H10Cl2N2O2/c1-13(15-2)9(14)12-6-3-4-7(10)8(11)5-6/h3-5H,1-2H3,(H,12,14)

Urea, 3-(3,4-dichlorophenyl)-1-methoxy-1-methyl-

Garnitan Herbicide 326Linuron

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 (~401.46 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (10.04 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.

---

Solubility in Formulation 2: ≥ 2.5 mg/mL (10.04 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.

---

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