Skeletal formula of tebufenpyrad
Space-filling model of the tebufenpyrad molecule
IUPAC name
Other names
119168-77-3 YesY
3D model (Jmol) Interactive image
ChemSpider 77872 N
ECHA InfoCard 100.122.745
KEGG C11126 YesY=  YesY
PubChem 86354
Molar mass 333.86 g·mol−1
Appearance White crystalline solid
Density 0.5 g/mL at 24.1 °C
Melting point 64 to 66 °C (147 to 151 °F; 337 to 339 K)
2.61 ppm at pH 5.9
3.21 ppm at pH 4
2.39 ppm at pH 7
2.32 ppm at pH 10
Acidity (pKa) 5.9 in water
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Infobox references

Tebufenpyrad is an insecticide and acaricide widely used in greenhouses. It is a white solid chemical with a slight aromatic smell. It is soluble in water and also in organic solvents.[2]

Mode of action

Tebufenpyrad is a strong mitochondrial complex I inhibitor. Like Rotenone, it inhibits electron transport chain by inhibiting the complex I enzymes of mitochondria which ultimately leads to lack of ATP production and finally cell death.


Tebufenpyrad is used mainly in greenhouses around the world. It has been registered under various trade names (i.e.Masai, Pyranica)[3] in countries like Australia, China and certain South American countries. It is registered in USA for use on ornamental plants in commercial green houses.[1]:1 The data available presented enough evidence to support unconditional registration of tebufenpyrad for use on ornamental plants in greenhouses.[1]:13

Exposure and toxicity

It is mainly used in greenhouses and the major form of exposure is through occupational exposure where this chemical is manufactured or used extensively. The possible routes of exposure are through inhalation or dermal exposure.[2] Since it is used in ornamental plants the exposure through food is limited. The LD 50 values for various laboratory animals are as follows: LD50 Rat (male) oral 595 mg/kg LD50 Rat (female) oral 997 mg/kg LD50 Mouse (male) oral 224 mg/kg LD50 Mouse (female) oral 210 mg/kg LD50 Rat dermal >2000 mg/kg[4]


Hydroxylation is the major and primary biotransformation of tebufenpyrad reported both in vivo and in vitro. Ethyl and tetra-butyl groups are the targets of hydroxylation. The alcohol groups are oxidized to carboxylic groups which can then be conjugated with other groups in vivo.[5] In rodent studies it was shown that 80% of the pesticide was absorbed mainly in the digestive system within 24 hours, the major metabolites being the hydroxylated forms. Most of the compound and its metabolites were excreted through feces and urine. There was no evidence of accumulation in the body of the rodents.[1]:11 The metabolites excreted out differed from male to female in rodents. While males excreted the carboxylic derivatives of the parent compound, the female rats excreted the sulfate conjugates of carboxylic acid. Interestingly, the Lethal Dose 50(LD50) values of male and female rats was very different. While the LD50 value of female rats was 997 mg/kg the LD50 for male rats was only 595 mg/kg.[4] This vast difference in LD 50 value might be attributed to this biotransformation.

Consequences of exposure

Tebufenpyrad exposure has been linked to cancer but to date no human data has been conclusive enough to link the two.[6] Recently this pesticide has been shown to affect the dopaminergic neuronal cell lines N27 by disrupting the mitochondrial dynamics. Loss of dopaminergic cells have been linked to Parkinson's disease in which the neuronal mitochondria are affected.[7] These findings may show that tebufenpyrad might also be able to affect the neurons. Overexposure of the pesticide has also lead to the development of resistance among different target organisms.[8] Recent studies have detected tebufenpyrad resistance in two spider mite species in apple trees in Western Australia.[9]


  1. 1 2 3 4 Tebufenpyrad Pesticide Fact Sheet, U.S. Environmental Protection Agency
  2. 1 2 http://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?dbs+hsdb:@term+@DOCNO+7271
  3. Richard T. Meister, Ed. (January 2012). Crop Protection Handbook 2012: The Essential Desktop Reference for Plant Health Experts. 98. Meister Publishing Company. p. 665. ISBN 978-1-892829-25-2.
  4. 1 2 MacBean C, ed. Tebufenpyrad (119168-77-3). In: The e-Pesticide Manual, 15th Edition, Version 5.0.1 (2011-2012). Surrey UK, British Crop Protection Council
  5. Casarett, Louis; Doull, John; Klaassen, Curtis (2001). Casarett and Doull's Toxicology: The Basic Science of Poisons (6th ed.). McGraw Hill Professional. p. 1193. ISBN 978-0-07-112453-9.
  6. USEPA Office of Pesticide Programs, Health Effects Division, Science Information Management Branch: "Chemicals Evaluated for Carcinogenic Potential" (April 2006)
  7. Charli, Adhithiya; Jin, Huajun; Anantharam, Vellareddy; Kanthasamy, Arthi; Kanthasamy, Anumantha G. (2015). "Alterations in mitochondrial dynamics induced by tebufenpyrad and pyridaben in a dopaminergic neuronal cell culture model". NeuroToxicology. doi:10.1016/j.neuro.2015.06.007. ISSN 0161-813X.
  8. Auger, Philippe; Bonafos, Romain; Guichou, Sabine; Kreiter, Serge (2003). "Resistance to fenazaquin and tebufenpyrad in Panonychus ulmi Koch (Acari: Tetranychidae) populations from South of France apple orchards". Crop Protection. 22 (8): 1039–1044. doi:10.1016/S0261-2194(03)00136-4. ISSN 0261-2194.
  9. Herron, G.A.; Rophail, J. (1998). "Tebufenpyrad (Pyranica®) resistance detected in two-spotted spider mite Tetranychus urticae Koch (Acari: Tetranychidae) from apples in Western Australia". Experimental & Applied Acarology. 22 (11): 633–641. doi:10.1023/A:1006058705429. ISSN 0168-8162.
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