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Development and use

Coumatetralyl is a first-generation hydroxycoumarin anticoagulant rodenticide that was developed in the 1950s. Along with warfarin, coumatetralyl was one of the compounds that dominated rodent control worldwide from 1950 to 1965 (Hadler and Buckle, 1992). The emergence of resistant rat and mouse strains in the UK, Europe and the USA caused a decline in coumatetralyl use, and stimulated the development of more potent second-generation anticoagulant rodenticides (Greaves and Ayres, 1969). Although it is unlikely to control warfarin-resistant strains (Rowe and Redfern, 1968), coumatetralyl is still registered in all Australian states and territories for controlling introduced rats and mice. Therefore, for effective control, users of coumatetralyl need to ensure that fresh bait is continually available.

Mode of action

Coumatetralyl exhibits the same mode of action as all anticoagulant rodenticides (Silverman, 1980). When a rodent eats the bait, the active anticoagulant blocks the epoxide reductase enzyme and stops the recycling of activated vitamin K. This severely reduces the production of blood-clotting factors. When the existing supply of clotting factors are eventually degraded, the clotting mechanism fails and haemorrhaging begins. As with all anticoagulants, there is a considerable delay between consumption of a lethal dose and the onset of symptoms. Effects develop progressively, and include haemorrhage, shock, loss of consciousness, and death (Petterino and Paolo, 2001).

Metabolism of coumatetralyl occurs faster than second-generation rodenticides. The compound persists in the liver of rodents, with a half-life of 55 days for rats (Parmar et al., 1987) and 16 days for mice (Vandenbroucke et al., 2008). Coumatetralyl is excreted primarily in the faeces and, to a lesser extent, in the urine of rodents. Therefore, rat droppings and rodent carcases should be cleared from production areas as soon as possible to reduce secondary poisoning risk. Due to its relatively short metabolic half-life, coumatetralyl (along with all first-generation anticoagulant rodenticides) is more effective if administered in small daily doses rather than a large single dose (Hadler and Buckle, 1992). Therefore, effective coumatetralyl application is likely to require greater total amounts and more frequent re-application of bait.

Time to death

  • Rats: 3–17 days (Bentley and Larthe, 1959; Hagan and Radomski, 1953; Lund, 1981; Hadler and Buckle, 1992)*
  • Mice: 3–21 days (Bentley and Larthe, 1959)*

*Time to death for rodents following ingestion of coumatetralyl is not explicitly reported in scientific literature. Because coumatetralyl has a shared mode of action and similar acute toxicity values, it is likely that the time to death is comparable to other first-generation anticoagulant rodenticides (namely, diphacinone and warfarin).

Evidence of resistance

Evidence of the existence of cross-resistance to all first-generation anticoagulants has been observed in Europe (Rowe and Redfern, 1965; Greaves and Ayres, 1969; Hadler and Shadbolt, 1975). To date, no resistance studies have been conducted in Australian pest rodent species.

APVMA-registered products containing coumatetralyl

Racumin (0.37g/kg), Racumin 8 (8g/kg), Ratex (0.38g/kg), Readi Rac (0.4g/kg), Surefire Couma (0.37g/kg)

Available formulations

  • Paste bait
  • Tracking powder
  • Wax block

Acute toxicity

SpeciesLD50Average bodyweightAmount of bait consumed for a LD50Reference (for LD50)
Mouse>1000mg/kg20g2.5–54g*Vandenbroucke et al., 2008
Norway rat16.5mg/kg320g0.66–14.3g*Tomlin, 2009
*Calculated using a bait concentration of 0.37–8g/kg

The table above shows the oral median lethal dose (LD50) values of coumatetralyl for the house mouse and Norway rat, the typical bodyweight for an adult animal from each species, and the total amount of commercial bait needed to be eaten to cause death. An adult rat (bodyweight of 320 grams) will eat about 20–30 grams of food daily, and an adult mouse (bodyweight of 20 grams) will eat 2–5 grams of food daily (Hadler and Buckle, 1991). Coumatetralyl rodenticides have a standard active concentration of 0.37–8g/kg. Therefore, 0.66–14.3 grams of bait would be considered a lethal dose for rats and 2.5–54 grams of bait is lethal for mice. For coumatetralyl products with a higher active concentration (8g/kg), this is within the daily feed requirements for rats and mice, and it is possible for a lethal dose to be consumed in a single feed. However, most products require repeated feeding of bait for effective control.

Poison schedule and regulatory requirements

Depending on the active concentration, coumatetralyl is either a Schedule 5 or Schedule 6 poison with a low to moderate potential for causing harm. Products containing coumatetralyl are required to have distinctive packaging with strong warnings and safety direction on the label. There are no special regulations restricting the availability, possession, storage or use of products containing coumatetralyl.

Handling, storage and user safety

Users are advised to wear gloves, safety glasses, and appropriate clothing to avoid skin and eye contact. Do not inhale dust. Do not touch the bait; use the scoop or measure. If it’s on skin and after each baiting, wash thoroughly with soap and water.

Containers that have been used to house bait should not be used for any other purpose. Store in tightly sealed original containers in a dry secure place away from fertilisers, seed, feed and food. Store out of direct sunlight. Keep out of reach of children, unauthorised persons and animals.

Read the label before use. For detailed instructions on handling and user safety, please refer to the relevant Safety Data Sheet.


Bentley, E. W. and Larthe Y. (1959). The comparative rodenticidal efficiency of five anti-coagulants. Journal of Hygiene, 57:135-149.

Hadler, M. R., & Buckle, A. P. (1992). Forty-five years of anticoagulant rodenticides—past, present and future trends. In Proceedings of the Fifteenth Vertebrate Pest Conference, 15.

Hadler, M. R., & Shadbolt, R.S. (1975). Novel 4-hydroxycoumarin anticoagulants active against resistant rats. Nature, 253:275-277.

Hagan, E. C. and Radomski, J. L. (1953). The toxicity of 3-(acetonylbenzyl)-4-hydroxycoumarin (warfarin) to laboratory animals. Journal of the American Pharmaceutical Association, 42:379-382.

Greaves, J. H. and Ayres, P. (1969). Some rodenticidal properties of coumatetralyl. Journal of Hygiene, 67:311-315.

Lund, M. (1981). Comparative effect of the three rodenticides warfarin, difenacoum and brodifacoum on eight rodent species in short feeding periods. Epidemiology & Infection, 87(1), 101-107.

Parmar, G., Bratt, H., Moore, R., & Batten, P. L. (1987). Evidence for common binding site in vivo for the retention of anticoagulants in rat liver. Human Toxicology, 6:431-432.

Petterino, C. and Paolo, B. (2001). Toxicology of various anticoagulant rodenticides in animals. Veterinary and Human Toxicology, 43:353-360.

Rowe, F. P. and Redfern, R. (1965). Toxicity tests on suspected warfarin resistant house mice (Mus musculus L.). Epidemiology & Infection, 63(3), 417-425.

Silverman, R.B. (1980). A model for the molecular mechanism of anticoagulant activity of 3-substituted 4-hydroxycoumarins. Journal of the American Chemical Society, 102(16), 5421-5423.

Thijssen, H. (1995). Warfarin-based rodenticides: Mode of action and mechanism of resistance. Pesticide Science, 43(1), 73-78.

Tomlin, C. 2009. The Pesticide Manual: A World Compendium. British Crop Production Council.

Vandenbroucke, V., Bousquet-Melou, A., De Backer, P., & Croubels, S. (2008). Pharmacokinetics of eight anticoagulant rodenticides in mice after single oral administration. Journal of veterinary pharmacology and therapeutics, 31(5), 437-445.

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