Strychnine (/ˈstrɪkniːn, -nɪn/, STRIK-neen, -⁠nin, US chiefly /-naɪn/ -⁠nyne)[6][7] is a highly toxic, colorless, bitter, crystalline alkaloid used as a pesticide, particularly for killing small vertebrates such as birds and rodents.

Strychnine, when inhaled, swallowed, or absorbed through the eyes or mouth, causes poisoning which results in muscular convulsions and eventually death through asphyxia.

[8] While it is no longer used medicinally, it was used historically in small doses to strengthen muscle contractions, such as a heart[9] and bowel stimulant[10] and performance-enhancing drug.

[15] The next step is hydrolysis of the acetal, which opens the ring by elimination of glucose (O-Glu) and provides a reactive aldehyde.

The nascent aldehyde is then attacked by a secondary amine to afford geissoschizine, a common intermediate of many related compounds in the Strychnos family.

Stereospecific reduction of the endocyclic double bond by NADPH and hydroxylation provides the Wieland-Gumlich aldehyde, which was first isolated by Heimberger and Scott in 1973, although previously synthesized by Wieland and Gumlich in 1932.

[18] An early synthetic chemist targeting strychnine, Robert Burns Woodward, quoted the chemist who determined its structure through chemical decomposition and related physical studies as saying that "for its molecular size it is the most complex organic substance known" (attributed to Sir Robert Robinson).

[23] The molecule has since received continuing wide attention in the years since for the challenges to synthetic organic strategy and tactics presented by its complexity; its synthesis has been targeted and its stereocontrolled preparation independently achieved by more than a dozen research groups since the first success.

When the inhibitory signals are prevented, the motor neurons are more easily activated and the victim has spastic muscle contractions, resulting in death by asphyxiation.

[29][30] Strychnine poisoning in animals usually occurs from ingestion of baits designed for use against gophers, rats, squirrels, moles, chipmunks and coyotes.

Birds affected by strychnine poisoning exhibit wing droop, salivation, tremors, muscle tenseness, and convulsions.

If a lower dose is ingested, other symptoms begin to develop, including seizures, cramping, stiffness,[44] hypervigilance, and agitation.

[32] As strychnine poisoning progresses, tachycardia (rapid heart beat), hypertension (high blood pressure), tachypnea (rapid breathing), cyanosis (blue discoloration), diaphoresis (sweating), water-electrolyte imbalance, leukocytosis (high number of white blood cells), trismus (lockjaw), risus sardonicus (spasm of the facial muscles), and opisthotonus (dramatic spasm of the back muscles, causing arching of the back and neck) can occur.

[54] Strychnine poisoning demands aggressive management with early control of muscle spasms, intubation for loss of airway control, toxin removal (decontamination), intravenous hydration and potentially active cooling efforts in the context of hyperthermia as well as hemodialysis in kidney failure (strychnine has not been shown to be removed by hemodialysis).

[61] Other sources specific to strychnine state that activated charcoal may be used after one hour of ingestion, depending on dose and type of strychnine-containing product.

These treatments involve keeping the patient in a quiet and darkened room,[65] anticonvulsants such as phenobarbital or diazepam,[55] muscle relaxants such as dantrolene,[66] barbiturates and propofol,[67] and chloroform or heavy doses of chloral, bromide, urethane or amyl nitrite.

[55] The sine qua non of strychnine toxicity is the "awake" seizure, in which tonic-clonic activity occurs but the patient is alert and oriented throughout and afterwards.

Due to slight protein binding, strychnine leaves the bloodstream quickly and distributes to bodily tissues.

[77] In persons killed by strychnine, the highest concentrations are found in the blood, liver, kidney and stomach wall.

The toxic and medicinal effects of Strychnos nux-vomica have been well known from the times of ancient India, although the chemical compound itself was not identified and characterized until the 19th century.

Strychnos nux-vomica is a tree native to the tropical forests on the Malabar Coast in Southern India, Sri Lanka and Indonesia, which attains a height of about 12 metres (39 ft).

The fruit has an orange color and is about the size of a large apple with a hard rind and contains five seeds, which are covered with a soft wool-like substance.

These seeds are the chief commercial source of strychnine and were first imported to and marketed in Europe as a poison to kill rodents and small predators.

Strychnine was first discovered by French chemists Joseph Bienaimé Caventou and Pierre-Joseph Pelletier in 1818 in the Saint-Ignatius' bean.

Historic records indicate that preparations containing strychnine (presumably) had been used to kill dogs, cats, and birds in Europe as far back as 1640.

One notorious instance of its use was during the 1904 Olympics marathon, when track-and-field athlete Thomas Hicks was unwittingly administered a concoction of egg whites and brandy laced with a small amount of strychnine by his assistants in a vain attempt to boost his stamina.