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Famphur, also known as Famophos, is an organothiophosphate insecticide which has been used on livestock to kill lice. The drug is an acetylcholine esterase inhibitor. Famphur was the active ingredient in Warbex, a pour-on cattle insecticide trademarked by American Cyanamid in 1965. Famphur is considered by the World Health Organisation as a highly to extremely hazardous (class I) pesticide.[1] The use of Famphur as a pesticide is restricted in the US [1], and it is not approved for use in the EU or UK.[2]

Chem info box

IUPAC name: 4-dimethoxyphosphinothioyloxy-N, N-dimethylbenzenesulfonamide

Synonyms: Famphur, Famophos, O-[4-(Dimethylsulfamoyl)phenyl]O,O-dimethyl phosphorothioate [3]

Properties [3]

• Appearance: Colourless crystalline powder
• Melting point: 52.5 - 53.5 °C
• Solubility in water: Sparing
• Vapour pressure: 0.00000136 [mmHg]
• LogP: 2.23

Hazard [3]

• GSH
• Pictograms
• Signal word: Danger
• Hazard Statements: H300, H312, H315, H319
• Precautionary Statements: P264, P264+P265, P270, P280, P301+P316, P302+P352, P305+P351+P338, P317, P321, P330, P332+P317, P337+P317, P362+P364, P405, and P501
• LD50 (rat, oral): 28 mg/kg

Famphur is produced through a multistep chemical synthesis. An important intermediate, dimethyl phosphorochloridothioate, is first prepared and serves as the phosphorus-containing core of the molecule. This intermediate reacts with 4-dimethylsulfamoylphenol via a nucleophilic substitution reaction, forming the O,O-dimethyl phosphorothioate ester characteristic of organophosphate pesticides.[4], [5]

Famphur is a synthetic organophosphate (thiophosphate) compound that acts as an acetylcholinesterase inhibitor. The compound inhibits the enzyme acetylcholinesterase by phosphorylating the active site serine residue of the enzyme. This prevents the hydrolysis of the neurotransmitter acetylcholine (ACh), leading to its accumulation at synapses and resulting in continuous stimulation of the nervous system.[6]

As mentioned, Famphur targets a group of enzymes called cholinesterases, which act as regulators of the neurotransmitter acetylcholine, affecting the nervous system and muscles [8], [9]. Different sensitivity of this enzyme to the toxin leads to different strengths of the effect between species. For example, mice are more strongly affected by the chemical than some insects, like cockroaches and milkweed bugs [9].The compound has no data on human exposure. Thus, most of the information relates to mammalian and insect studies.

Administration to livestock can be by intramuscular or subcutaneous injection, through the diet, as a dermal pour-on, or as an oral bolus. In sheep, Famphur is well excreted if introduced to the blood circulation intravenously, with small amounts being present in tissues. Nearly all of the compound gets excreted via urine or faecal elimination [3]. However, intramuscular administration results in substantially slower excretion, due to delayed release of the compound from the injection site into the bloodstream. Overall, the compound is rapidly metabolised by mammals, with a half-life investigated in cattle – 0.9 days (using a single dermal pour-on method) [7].

In one study, Famphur was radioactively labelled to investigate the most important sites of excretion and distribution of the compound and its metabolites [9]. The results showed high radioactivity levels in the kidneys and bile, suggesting that they are vital for the elimination of the compound and its metabolites.

Most of Famphur’s metabolites do not possess significant danger except for famoxon, which could potentially increase health risks when injected intravenously [9].

As an organophosphorus (OP) derivative, Famphur acts by irreversibly inhibiting and inactivating the enzyme acetylcholinesterase (AChE) [3]. Inhibition of AChE halts the breakdown of acetylcholine (ACh) to choline and acetic acid, leading to an excess level of ACh in the cholinergic synapses[6].

In insects using ACh as a primary neurotransmitter, exposure to OPs leads to instant death due to the overstimulation of the receptors in their nervous system [7], [8], [9]. In humans, a drastic increase in ACh levels could cause respiratory failure by leading to overstimulation of muscarinic and nicotinic receptors, as well as the central nervous system [2]. Furthermore, evidence shows that acute exposure to OPs in rats can lead to Status Epilepticus (SE), a main cause of the development of neuronal degeneration [2].

OPs can still trigger neurological damage, even at doses that are too low to inhibit AChE and still disrupt processes like axonal transport or induce oxidative stress and mitochondrial effects[10]. Another connection is also made between acute exposure to OPs and neuroinflammation and damage that could induce Alzheimer's disease[11].

Pesticides containing Famphur are approved to be used on cattle as a pour-on insecticide and for medicated feed. Famphur is an active ingredient of TRAMISOL X-TRA Combination Paste, which targets "Stomach worms (Haemonchus, Trichostrongylus, Ostertagia), intestinal worms (Trichostrongylus, Cooperia, Nematodirus, Bunostomum, Oesophagostomum), lungworms (Dictyocaulus), cattle grubs (Hypoderma), biting lice (Bovicola), and sucking lice (Linognathus, Solenoptes)."

Famphur is classified as a Group D compound, meaning that there is insufficient evidence to determine whether it is carcinogenic to humans.[2]

The toxicity of Famphur varies depending on the species and route of exposure. Famphur can cause severe toxicity at relatively low doses, particularly in mammals.

In humans, exposure to Famphur can occur through several routes, such as oral ingestion and through dermal exposure.

Famphur is considered harmful or potentially fatal if swallowed or absorbed through the skin. Dermal absorption can vary depending on the solvent present.[2] For example, studies using rat skin have shown that acetone has rapid skin penetration, while substances such as corn oil or benzene have a slower penetration.[12]

Famphur can cause toxic effects in a wide range of organisms. During metabolism, Famphur is converted into several compounds, including famoxon, which is one of the most toxic metabolites.[13] Other metabolites are generally less toxic.[14]

Studies have shown that Famphur can cause mortality in mammals, birds, and other wildlife at relatively low concentrations. Based on toxicity classifications, Famphur is considered highly toxic for many bird species and is considered a Class-II compound for Japanese quail.[15]

Famphur is rapidly metabolised in animals, but residues can still be detected in tissues and milk.[16] Long-term observations have suggested potential delayed physiological effects. For example, alterations in blood chemistry were reported in reindeer.[2], [17]

In LD50 studies of mammals, including domestic animals (goat and sheep), Famphur was shown to trigger behavioural effects mainly, somnolence, convulsions, seizures, or abnormal food intake, as well as more severe conditions like muscle contractions or respiratory abnormalities.[3]

Before discovering the dangers of Famphur, it was applied by veterinarians on cattle using a pour-on method. When this process was occurring in poorly ventilated spaces, people reported symptoms like nausea, headaches, and irritation of the throat and facial skin.  No decrease in blood cholinesterase activity was observed.[3]

Another study has suggested that there might be a significant risk for leukaemia in farmers exposed to a group of chemicals in which Famphur was present. However, there is no concrete evidence that leukaemia can be caused by Famphur.[18]

[1]        ‘MPS-List prohibited active substances’, MPS, P052024. [Online]. Available: content/uploads/2022/11/MPS-List-prohibited-active-substances-2024-2025.pdf

[2]        Ronald Eisler, ‘Famphur Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review’, U.S. Department of the Interior National Biological Survey Washington, D.C. 20240, 27, Feb. 1994. [Online]. Available: https://scispace.com/pdf/famphur-hazards-to-fish-wildlife-and-invertebrates-a-15i7w7287r.pdf

[3]        PubChem, ‘NIH - Famphur’. Accessed: Mar. 02, 2026. [Online]. Available: https://pubchem.ncbi.nlm.nih.gov/compound/5859

[4]        WH23, Famphur Synthesis. 2022. Accessed: Mar. 06, 2026. [Online]. Available: https://commons.wikimedia.org/wiki/File:Famphur_Synthesis.svg

[5]        Agriculture & Environment Research Unit, University of Hertfordshire, ‘Pesticide Properties DataBase - Famphur’, Pesticide Properties DataBase (PPDB). Accessed: Mar. 06, 2026. [Online]. Available: https://sitem.herts.ac.uk/aeru/vsdb/Reports/1598.htm

[6]        V. Aroniadou-Anderjaska, T. H. Figueiredo, M. de Araujo Furtado, V. I. Pidoplichko, and M. F. M. Braga, ‘Mechanisms of Organophosphate Toxicity and the Role of Acetylcholinesterase Inhibition’, Toxics, vol. 11, no. 10, p. 866, Oct. 2023, doi: 10.3390/toxics11100866.

[7]        J. E. Casida and K. A. Durkin, ‘Anticholinesterase insecticide retrospective’, Chem Biol Interact, vol. 203, no. 1, pp. 221–225, Mar. 2013, doi: 10.1016/j.cbi.2012.08.002.

[8]        H. Breer, W. Hanke, D. Benke, E. Tareilus, and J. Krieger, ‘Nicotinic Acetylcholine Receptors in the Nervous System of Insects’, in Molecular Biology of Neuroreceptors and Ion Channels, A. Maelicke, Ed., Berlin, Heidelberg: Springer, 1989, pp. 55–68. doi: 10.1007/978-3-642-74155-5_5.

[9]        S. H. Thany and H. Tricoire-Leignel, ‘Emerging Pharmacological Properties of Cholinergic Synaptic Transmission: Comparison between Mammalian and Insect Synaptic and Extrasynaptic Nicotinic Receptors’, Curr Neuropharmacol, vol. 9, no. 4, pp. 706–714, Dec. 2011, doi: 10.2174/157015911798376343.

[10]      Y. Chen et al., ‘Mechanisms of Neurotoxicity of Organophosphate Pesticides and Their Relation to Neurological Disorders’, NDT, vol. 20, pp. 2237–2254, Nov. 2024, doi: 10.2147/NDT.S479757.

[11]      B. Yadav et al., ‘Implications of organophosphate pesticides on brain cells and their contribution toward progression of Alzheimer’s disease’, Journal of Biochemical and Molecular Toxicology, vol. 38, no. 3, p. e23660, 2024, doi: 10.1002/jbt.23660.

[12]      R. D. O’Brien and C. E. Dannelley, ‘Insecticide Toxicity, Penetration of Insecticides through Rat Skin’, J. Agric. Food Chem., vol. 13, no. 3, pp. 245–247, May 1965, doi: 10.1021/jf60139a014.

[13]      P. E. Gatterdam, L. A. Wozniak, M. W. Bullock, G. L. Parks, and J. E. Boyd, ‘Absorption, Metabolism, and Excretion of Tritium-Labeled Famphur in the Sheep and Calf’, J. Agric. Food Chem., vol. 15, no. 5, pp. 845–853, May 1967, doi: 10.1021/jf60153a036.

[14]      K. Kaemmerer and S. Buntenkötter, ‘The problem of residues in meat of edible domestic animals after application or intake of organophosphate esters’, F. A. Gunther and J. D. Gunther, Eds, Berlin, Heidelberg: Springer Berlin Heidelberg, 1973, pp. 1–240. doi: 10.1007/978-3-662-40267-2_1.

[15]      E. F. Hill and M. B. Camardese, ‘Lethal Dietary Toxicities of Environmental Contaminants and Pesticides to Coturnix’, U.S. Fish and Wildlife Service, No. 2, 1986. Accessed: Mar. 14, 2026. [Online]. Available: https://pubs.usgs.gov/publication/5230190

[16]      A. Annand, J. Dingle, A. Heath, and W. Palmer, ‘Residues of famphur in bovine tissues and milk following its application as a pour-on insecticide’, Australian Journal of Experimental Agriculture and Animal Husbandry, vol. 16, no. 78, pp. 82–87, Feb. 1976, doi: 10.1071/EA9760082.

[17]      M. C. Ivey, J. S. Palmer, and R. H. Washburn, ‘Famphur and its oxygen analogue: residues in the body tissues of reindeer’, J Econ Entomol, vol. 69, no. 2, pp. 260–262, Apr. 1976, doi: 10.1093/jee/69.2.260.

[18]      L. M. Brown et al., ‘Pesticide Exposures and Other Agricultural Risk Factors for Leukemia among Men in Iowa and Minnesota’, Cancer Res, vol. 50, no. 20, pp. 6585–6591, Oct. 1990.