[5] Another approach is to develop targeted drugs (which, unlike antibodies, are usually synthetic and easier to manufacture at scale).

[1] In the US, approved antivenom, including for pit viper (rattlesnake, copperhead and water moccasin) snakebite, is based on a purified product made in sheep known as CroFab.

[11][12] As an alternative when conventional antivenom is not available, hospitals sometimes use an intravenous version of the antiparalytic drug neostigmine to delay the effects of neurotoxic envenomation through snakebite.

[13] Some promising research results have also been reported for administering the drug nasally as a "universal antivenom" for neurotoxic snakebite treatment.

[20] The host animals may include horses, donkeys, goats, sheep, rabbits, chickens, llamas, and camels.

The use of serum from immunized animals as a treatment for disease was pioneered in 1890 by Emil von Behring and Shibasaburo Kitasato, who first demonstrated that the infectious diseases diphtheria and tetanus could be prevented or cured using transfusions from an immune animal to a susceptible one.

[23] On February 10, 1894, Albert Calmette at the Pasteur Institute, and independently Césaire Auguste Phisalix and Gabriel Bertrand at the National Museum of National History in France, announced that they had achieved the same result—treatment of a vulnerable animal with serum from an immunized one—this time using snake venom as the source of protection and disease.

[27] Surgeon-Major Edward Nicholson wrote in the November 1870 Madras Medical Journal that he had witnessed a Burmese snake-catcher inoculating himself with cobra venom.

In 1895 Sir Thomas Fraser, Professor of Medicine at the University of Edinburgh, picked up Fayrer and Waddell's research to produce a serum to act against cobra venom.

His "antivenene" was effective in the laboratory, but failed to make an impact as the public were focused on contemporary Pasteurian discoveries.

[29] In 1901, Vital Brazil, working at the Instituto Butantan in São Paulo, Brazil, developed the first monovalent and polyvalent antivenoms for Central and South American Crotalus and Bothrops genera,[30] as well as for certain species of venomous spiders, scorpions, and frogs.

In Mexico in 1905, Daniel Vergara Lope developed an antivenom against scorpion venom, by immunizing dogs.

[34] Over time, a variety of improvements have been made in the specificity, potency, and purity of antivenom products, including "salting out" with ammonium sulphate or caprylic acid,[35] enzymatic reduction of antibodies with papain or with pepsin, affinity purification, and a variety of other measures.

[40] When weighed against profitability (especially for sale in poorer regions), the result is that many snake antivenoms, world-wide, are very expensive.

[50] In 1981, the World Health Organization decided that the preferred terminology in the English language would be venom and antivenom rather than venin and antivenin or venen and antivenene.