Colorado River Toad

1. Review Article
Colorado River Toad
(Psychoactive Toad)
By Mahdy Ali Ahmad Osman ,B.Pharm.,
Pharm.D., PGDPhV
Email:mahady_333@yahoo.com
The Colorado River toad (Incilius
alvarius), also known as the Sonoran
Desert toad, is a psychoactive toad found
in northern Mexico and the southwestern
United States. Its toxin, as an exudates of
glands within the skin, contains 5-MeO-
DMT and bufotenin.
Bufotenin, (5-HO-DMT,N,N
dimethylserotonin, bufotenine) is a
tryptamine related to the
neurotransmitter serotonin. It is an
alkaloid . Bufotenin is similar in chemical
structure to the psychedelics psilocin (4-
HO-DMT), 5-MeO-DMT, and DMT,
chemicals which also occur in some of the
same fungus, plant, and animal species as
bufotenin.
The psychoactivity of bufotenin has been
disputed, though recent studies suggest it
is similar in nature to 5-MeO-DMT.
The Colorado River toad can grow to
about 190 millimetres (7.5 in) long, it has
a smooth, leathery skin and is olive green
or mottled brown in color. Just behind the
large golden eye with horizontal pupil is a
bulging kidney-shaped parotoid gland.
Toads in the family bufonidae have a
region of skin known as "the seat patch",
which extends from mid abdomen to the
hind legs and is specialized for rapid
rehydration. Most of the rehydration is
done through absorption of water from
small pools or wet objects.
History
Bufotenin was first isolated from toad
skin, and named by the Austrian chemist
Handovsky at the University of Prague
during World War I. The structure of
bufotenine was first confirmed in 1934 by
Heinrich Wieland’s laboratory in Munich,
and the first reported synthesis of
bufotenine was by Toshio Hoshino and
Kenya Shimodaira in 1935.
Breeding
The breeding season starts in May, when
the rainy season begins, and can last up to
August.
Drug use of poison
The toad's primary defense system are
glands that produce a poison that may be
potent enough to kill a grown dog. These

2. parotoid glands also produce the 5-MeO-
DMT and bufotenin for which the toad is
known; both of these chemicals belong to
the family of hallucinogenic tryptamines.
5-MeO-DMT may be smoked and is
powerfully psychoactive. After inhalation,
the user usually experiences a warm
sensation, euphoria, and strong visual and
auditory hallucinations. No long-lasting
effects have been reported.
Pharmacokinetic
In rats, subcutaneously administered
bufotenin (1–100 μg/kg) distributes
mainly to the lungs, heart, and blood, and
to a much lesser extent, the brain
(hypothalamus, brain stem, striatum, and
cerebral cortex) and liver. It reaches peak
concentrations at 1 hour and is nearly
completely eliminated within 8 hours. In
humans, intravenous administration of
bufotenin results in excretion of (70%) of
injected drug in the form of 5-HIAA, an
endogenous metabolite of serotonin,
while roughly 4% is eliminated
unmetabolized in the urine. Orally
administered bufotenine undergoes
extensive first-pass metabolism by the
enzyme monoamine oxidase.
Lethal dose
The acute toxicity (LD50) of bufotenin in
rodents has been estimated at 200 to
300 mg/kg. Death occurs by respiratory
arrest. In April 2017 a South Korean man
died of bufotenin poisoning after
consuming toads that had been mistaken
as edible Asian bullfrogs.
Legal status
Australia
Bufotenin is classified as a Schedule I
controlled substance according to the
Criminal Code Regulations of the
Government of the Commonwealth of
Australia.
United Kingdom
In the UK, bufotenin is a Class A drug
under the 1971 Misuse of Drugs Act.
United States
Bufotenine (DEA Drug Code 7403) is
regulated as a Schedule I drug by the Drug
Enforcement Administration at the
federal level in the United States and is
therefore illegal to buy, possess, and sell.
Association with schizophrenia and
other mental disorders
A study conducted in the late 1960s
reported the detection of bufotenin in the
urine of schizophrenic subjects; however,
subsequent research has failed to confirm
these findings.
Studies have detected endogenous
bufotenin in urine specimens from
individuals with other psychiatric
disorders, such as infant autistic patients.
Another study indicated that paranoid
violent offenders or those who committed
violent behaviour towards family
members have higher bufotenin levels in
their urine than other violent offenders.
A 2010 study utilized a mass
spectrometry approach to detect levels of
bufotenin in the urine of individuals with
severe autism spectrum disorder (ASD),
schizophrenia, and asymptomatic

3. subjects. Their results indicate
significantly higher levels of bufotenin in
the urine of the ASD and schizophrenic
groups when compared to asymptomatic
individuals.
References
 Gowda RM, Cohen RA, Khan IA. Toad
venom poisoning: resemblance to digoxin
toxicity and therapeutic implications.
Heart. 2003 Apr 1;89(4):e14-.
 Moretti C, Gaillard Y, Grenand P, Bévalot
F, Prévosto JM. Identification of 5-
hydroxy-tryptamine (bufotenine) in
takini (Brosimumacutifolium Huber
subsp. acutifolium CC Berg, Moraceae), a
shamanic potion used in the Guiana
Plateau. Journal of ethnopharmacology.
2006 Jun 30;106(2):198-202.
 Chamakura RP. Bufotenine-A
Hallucinogen in Ancient Snuff Powders of
South America and a Drug of Abuse on the
Streets of New York City. Forensic science
review. 1994 Jun;6(1):1-8.
 Fuller RW, Snoddy HD, Perry KW. Tissue
distribution, metabolism and effects of
bufotenine administered to rats.
Neuropharmacology. 1995 Jul
31;34(7):799-804.
 Torres CM, Repke DB. Anadenanthera:
visionary plant of ancient South America.
Psychology Press; 2006.
 South Korean man dies after eating
toads". BBC. 21 April 2017.
 Faurbye A, Pind K. Occurrence of
bufotenin in the urine of schizophrenic
patients and normal persons. Nature.
1968 Nov 2;220(5166):489-.
 Siegel M. A senstive method for the
detection of N, N-dimethylserotonin
(bufotenin) in urine; failure to
demonstrate its presence in the urine of
schizophrenic and normal subjects.
Journal of psychiatric research. 1965 Oct
31;3(3):205-11.
 Pomilio AB, Vitale AA, Ciprian-Ollivier J,
Cetkovich-Bakmas M, Gómez R, Vázquez
G. Ayahoasca: an experimental psychosis
that mirrors the transmethylation
hypothesis of schizophrenia. Journal of
ethnopharmacology. 1999 Apr
1;65(1):29-51.
 Ciprian-Ollivier J, Cetkovich-Bakmas MG.
Altered consciousness states and
endogenous psychoses: a common
molecular pathway?. Schizophrenia
research. 1997 Dec 19;28(2):257-65.
 Carpenter WT, Fink EB, Narasimhachari
N, Himwich HE. A test of the
transmethylation hypothesis in acute
schizophrenic patients. The American
journal of psychiatry. 1975 Oct.
 Takeda N. Serotonin-degradative
pathways in the toad (Bufo bufo
japonicus) brain: clues to the
pharmacological analysis of human
psychiatric disorders. Comparative
Biochemistry and Physiology Part C:
Pharmacology, Toxicology and
Endocrinology. 1994 Feb 1;107(2):275-
81.
 Räisänen M, Virkkunen M, Huttunen M,
Furman B, Kärkkäinen J. Increased
urinary excretion of bufotenin by violent
offenders with paranoid symptoms and
family violence. The Lancet. 1984 Sep
22;324(8404):700-1.
 Emanuele E, Colombo R, Martinelli V,
Brondino N, Marini M, Boso M, Barale F,
Politi P. Elevated urine levels of
bufotenine in patients with autistic
spectrum disorders and schizophrenia.
Neuroendocrinol Lett. 2010 Jan
1;31(1):117-21.
 Criminal Code Regulation 2005 (SL2005-
2) (rtf), Australian Capital Territory, May
1, 2005, retrieved 2007-08-12.
 Poisons Standard October 2015
https://www.comlaw.gov.au/Details/F20
15L01534.
 Poisons Act 1964. slp.wa.gov.au.
 Misuse of Drugs Act 1981 (2015).
slp.wa.gov.au.
 §1308.11 Schedule I.
deadiversion.usdoj.gov.