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57-24-9 (base) YesY
60-41-3 (sulfate) YesY
ChEBI CHEBI:28973 YesY
ChEMBL ChEMBL227934 YesY
ChEMBL612118 YesY
ChEMBL486399 YesY
ChemSpider 389877 YesY
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KEGG C06522 YesY
PubChem 441071
Molar mass 334.42 g·mol−1
Appearance white or translucent crystal or crystalline powder; Bitter tasting
Odor Odorless
Density 1.36 g cm−3
Melting point 543 K (270 °C)
0.02% (20°C)[1]
Acidity (pKa) 8.25[2]
Lethal dose or concentration (LD, LC):
0.5 mg/kg (dog, oral)
0.5 mg/kg (cat, oral)
2 mg/kg (mouse, oral)
16 mg/kg (rat, oral)
2.35 (rat, oral)[3]
0.6 mg/kg (rabbit, oral)[3]
US health exposure limits (NIOSH):
TWA 0.15 mg/m3[1]
TWA 0.15 mg/m3[1]
3 mg/m3[1]
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Infobox references

Strychnine (/ˈstrɪknn/; also US /ˈstrɪknn/ or /ˈstrɪknɪn/) 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 eyes or mouth, causes a poisoning which results in muscular convulsions and eventually death through asphyxia.[4] While it has no known medicinal effects, in the past the convulsant effect was believed to be beneficial in small doses. The most common source is from the seeds of the Strychnos nux-vomica tree.


Strychnine was the first alkaloid to be identified in plants of the genus Strychnos, family Loganiaceae. Strychnos, named by Carl Linnaeus in 1753, is a genus of trees and climbing shrubs of the gentian order. The genus contains 196 various species and is distributed throughout the warm regions of Asia (58 species), America (64 species), and Africa (75 species). The seeds and bark of many plants in this genus contain the powerful poison strychnine.


Strychnine was first discovered by French chemists Joseph Bienaimé Caventou and Pierre-Joseph Pelletier in 1818 in the Saint-Ignatius' bean.[5] In some Strychnos plants a 9,10-dimethoxy derivative of strychnine, the alkaloid brucine, is also present. Brucine is not as poisonous as strychnine. Historic records indicate that preparations containing strychnine (presumably) had been used to kill dogs, cats, and birds in Europe as far back as 1640.[6] The structure of strychnine was first determined in 1946 by Sir Robert Robinson and in 1954 this alkaloid was synthesized in a laboratory by Robert B. Woodward. This is one of the most famous syntheses in the history of organic chemistry. Both chemists won the Nobel prize (Robinson in 1947 and Woodward in 1965).[6]

Performance enhancer[edit]

Strychnine was popularly used as an athletic performance enhancer and recreational stimulant in the late 19th Century and early 20th Century, due to its convulsant effects. It was thought to be similar to coffee.[7][8] Its effects are well described in H. G. Wells' novella The Invisible Man: the title character states: " Strychnine is a grand tonic ... to take the flabbiness out of a man." The protagonist replies: "It's the devil, ... It's the palaeolithic in a bottle."[9]


In high doses, strychnine is very toxic to humans and many other animals (LD50 = 0.16 mg/kg in rats, 1–2 mg/kg orally in humans[10]), and poisoning by inhalation, swallowing or absorption through eyes or mouth can be fatal.[citation needed] S. nux-vomica seeds are generally effective only when they are crushed or chewed before swallowing because the pericarp is quite hard and indigestible; poisoning symptoms may therefore not appear if the seeds are ingested whole.[citation needed]

Animal toxicity[edit]

Strychnine poisoning in animals usually occurs from ingestion of baits designed for use against gophers, moles and coyotes. Strychnine is also used as a rodenticide, but is not specific for such unwanted pests and may kill other small animals. In the United States, most baits containing strychnine have been replaced with zinc phosphide baits since 1990. In the Netherlands rodenticides with strychnine are forbidden.


The LD50 values for strychnine in animals
Organism Route LD50 (mg/kg)
Bird-wild[11] Oral 16
Cat[12] Intravenous 0.33
Cat[13] Oral 0.5
Dog[14] Intravenous 0.8
Dog[12] Subcutaneous 0.35
Dog[13] Oral 0.5
Duck[11] Oral 3.0
Mouse[15] Intraperitoneal 0.98
Mouse[16] Intravenous 0.41
Mouse[17] Oral 2.0
Mouse[18] Parenteral 1.06
Mouse[19] Subcutaneous 0.47
Pigeon[11] Oral 21.0
Quail[11] Oral 23.0
Rabbit[14] Intravenous 0.4
Rabbit[12] Oral 0.6
Rat[20] Oral 16.0
Rat[21] Oral 2.35

Human toxicity[edit]

The symptoms of poisoning in humans are generally similar to those as in other animals, because the mechanism of action is apparently similar across species. The toxicity of strychnine in humans is not ethically studied[citation needed], so most information known comes from cases of strychnine poisoning, unintentional and deliberate.

The following symptoms are indicative of a lethal dose:

  1. Severe nausea, including vomiting
  2. Convulsions of all muscle groups, which become longer and more closely spaced with time
  3. Spasms of the facial muscles, causing cyanosis of the face, dilated pupils, prominent eyeballs, and frothing at the mouth
  4. The body may exhibit the following "arching"/"bridging" postures:
    1. Opisthotonus: Hyperextension. The person may be resting on heels and occiput.
    2. Emprosthotonos: The spasm of abdominal muscles may bend the body forward.
    3. Pleurothotonus: The body may be flexed to one side.
  5. Loss of consciousness and a clear mind
  6. Immense reflex sensitivity (dramatic exaggeration of normal reflexes)
  7. Death due to asphyxiation, caused by muscle spasms[4]


The LD50 values for strychnine in humans
Route LD50 (mg)
Human[22][23] Oral 100–120
Human[24] Oral 30–60
Human (child)[25][26][27] Oral 15
Human (adult)[28] Oral 50–100
Human (adult)[27] Oral 30–100
Human (adult)[26] Oral 30
Human[29] Intravenously 5–10 (approximate)

For occupational exposures to strychnine, the Occupational Safety and Health Administration and National Institute for Occupational Safety and Health have set exposure limits at 0.15 mg/m3 over an 8-hour work day.[30]

Because strychnine produces some of the most dramatic and painful symptoms of any known toxic reaction, strychnine poisoning is often portrayed in literature and film.[citation needed]


strychnine biosynthesis

Strychnine is a terpene indole alkaloid belonging to the Strychnos family of Corynanthe alkaloids, and it is derived from tryptamine and secologanin.[31][32] The enzyme, strictosidine synthase, catalyzes the condensation of tryptamine and secologanin, followed by a Pictet-Spengler reaction to form strictosidine.[33] While the enzymes that catalyze the following steps have not been identified, the steps have been inferred by isolation of intermediates from Strychnos nux-vomica.[34] 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.[31]

A reverse Pictet-Spengler reaction cleaves the C2-C3 bond, while a subsequent Mannich reaction forms the C3-C7 bond, and a Michael addition forms the C2-C16 bond to provide dehydropreakuammicine. Hydrolysis of the methyl ester and decarboxylation leads to norfluorocurarine. 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.[34][35] To elongate the appendage by 2 carbons, acetyl-CoA is added to the aldehyde in an aldol reaction to afford prestrychnine. Strychnine is then formed by a facile addition of the amine with the carboxylic acid or its activated CoA thioester, followed by ring-closure via displacement of an activated alcohol.

Chemical synthesis[edit]

As early researchers have noted, the strychnine molecular structure, with its specific array of rings, stereocenters, and nitrogen functional groups is a complex synthetic target, and has stimulated interest for that reason and for interest in the structure-activity relationships underlying its pharmacologic activities.[36] An early synthetic chemist targeting strychnine, R.B. 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).[37]

The first total synthesis of strychnine was reported by the research group of R. B. Woodward in 1954, and is considered a classic in this field.[38][page needed][39] The Woodward account published in 1954 was very brief (3 pp.),[40] but was followed by a 42-page report in 1963.[41] 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 (see main strychnine total synthesis article).



Strychnine may be introduced into the body orally, by inhalation, or by injection. It is a potently bitter substance, and in humans has been shown to activate bitter taste receptors TAS2R10 and TAS2R46.[42][43][44] Strychnine is rapidly absorbed from the gastrointestinal tract.[citation needed]







Mechanism of action[edit]

Strychnine is a neurotoxin which acts as an antagonist of glycine and acetylcholine receptors. It primarily affects the motor nerves in the spinal cord which control muscle contraction. An impulse is triggered at one end of a nerve by the binding of neurotransmitters to the receptors. In the presence of a neuroinhibitor, such as glycine, a greater quantity of excitatory neurotransmitters must bind to receptors before there will be an action potential generated. Glycine acts primarily as an agonist of the glycine receptor, which is a ligand-gated chloride channel in neurons located in the spinal cord and in the brain. This chloride channel will allow the negatively charged chloride ions into the neuron, causing a hyperpolarization which pushes the membrane potential further from threshold. Strychnine is an antagonist of glycine, which means it binds to the same receptor, preventing the inhibitory effects of glycine on the postsynaptic neuron. Therefore, action potentials are triggered with lower levels of excitatory neurotransmitters. When the inhibitory signals are prevented, the motor neurons are more easily activated and the victim will have spastic muscle contractions, resulting in death by asphyxiation.[4][45] Structure of strychnine in complex with ACh binding protein (AChBP).[46]


There is no specific antidote for strychnine but recovery from strychnine exposure is possible with early hospital treatment. Treatment consists of removing the drug from the body (decontamination) and getting supportive medical care in a hospital setting. Supportive care includes intravenous fluids, medications against convulsions and spasms, and cooling measures for high temperature. The patient should be kept in a quiet and darkened room, because excessive manipulation and loud noises may cause convulsions. Because these convulsions are extremely painful, an appropriate painkiller should be given. Treatment of strychnine poisoning involves an oral administration of activated charcoal which adsorbs any strychnine within the digestive tract. Unabsorbed strychnine can be removed from the stomach by gastric lavage with tannic acid or potassium permanganate solutions to oxidize strychnine. Seizures are controlled by anticonvulsants, such as phenobarbital or diazepam, along with muscle relaxants such as dantrolene to combat muscle rigidity. Chloroform or heavy doses of chloral, bromide, urethane or amyl nitrate can also be used to restrain the convulsions. Because diazepam, as the anticonvulsant of choice, is not effective in all cases, a combination with midazolam, fentanyl, or pancuronium is recommended for controlling the convulsions. Strychnine poisoning demands an aggressive management with early intubation, control of muscle tremors, and prevention of rhabdomyolysis and renal failure. If the patient survives the first 24 hours after poisoning then recovery is probable.

Also, George Harley (1829–1896) showed in 1850 that Curare (wourali) was effective for the treatment of tetanus and strychnine poisoning.

See also[edit]


  2. ^ Everett, A. J.; Openshaw, H. T.; Smith, G. F. (1957). "221. The constitution of aspidospermine. Part III. Reactivity at the nitrogen atoms, and biogenetic considerations". Journal of the Chemical Society (Resumed): 1120. doi:10.1039/JR9570001120. 
  3. ^ a b "Strychnine". Immediately Dangerous to Life and Health. National Institute for Occupational Safety and Health (NIOSH). 
  4. ^ a b c Sharma, R.K., Consice textbook of forensic medicine & toxicology, Elsevier, 2008
  8. ^
  9. ^ H. G. Wells, The Invisible Man
  10. ^ INCHEM: Chemical Safety Information from Intergovernmental Organizations:Strychnine.
  11. ^ a b c d Tucker, RK; Haegele, MA (1971). "Comparative acute oral toxicity of pesticides to six species of birds". Toxicology and applied pharmacology 20 (1): 57–65. doi:10.1016/0041-008X(71)90088-3. PMID 5110827. 
  12. ^ a b c RTECS (1935)
  13. ^ a b Moraillon, R.; Pinoult, L. (1978). "Diagnostic et traitement d'intoxications courantes des carnivores". Rec Med Vet (in French) 174 (1–2): 36–43. 
  14. ^ a b Longo, V.G.; Silvestrini, B.; Bovet, D. (1959). "An investigation of convulsant properties of the 5,7-diphenyl-1,3-diazadamantan- 6-ol (IS 1757)". J. Pharmacol. Exp. Ther. 126 (1): 41–9. PMID 13642285. 
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