NOREPINEPHRINE (NE), also called NORADRENALINE (NA) or NORADRENALIN,
is an organic chemical in the catecholamine family that functions in
the brain and body as a hormone and neurotransmitter . The name
"noradrenaline," derived from Latin roots meaning "at/alongside the
kidneys," is more commonly used in the United Kingdom; in the United
States, "norepinephrine," derived from Greek roots having that same
meaning, is usually preferred. "Norepinephrine" is also the
international nonproprietary name given to the drug . Regardless of
which name is used for the substance itself, parts of the body that
produce or are affected by it are referred to as NORADRENERGIC.
In the brain, norepinephrine is produced in nuclei that are small yet
exert powerful effects on other brain areas. The most important of
these nuclei is the locus coeruleus , located in the pons . Outside
the brain, norepinephrine is used as a neurotransmitter by sympathetic
ganglia located near the spinal cord or in the abdomen , and it is
also released directly into the bloodstream by the adrenal glands .
Regardless of how and where it is released, norepinephrine acts on
target cells by binding to and activating noradrenergic receptors
located on the cell surface.
The general function of norepinephrine is to mobilize the brain and
body for action.
Norepinephrine release is lowest during sleep, rises
during wakefulness, and reaches much higher levels during situations
of stress or danger, in the so-called fight-or-flight response . In
the brain, norepinephrine increases arousal and alertness, promotes
vigilance, enhances formation and retrieval of memory, and focuses
attention; it also increases restlessness and anxiety. In the rest of
the body, norepinephrine increases heart rate and blood pressure ,
triggers the release of glucose from energy stores, increases blood
flow to skeletal muscle , reduces blood flow to the gastrointestinal
system, and inhibits voiding of the bladder and gastrointestinal
A variety of medically important drugs work by altering the actions
of norepinephrine systems.
Norepinephrine itself is widely used as an
injectable drug for the treatment of critically low blood pressure.
Beta blockers , which counter some of the effects of norepinephrine,
are frequently used to treat glaucoma , migraine , and a range of
cardiovascular problems. Alpha blockers , which counter a different
set of norepinephrine effects, are used to treat several
cardiovascular and psychiatric conditions. Alpha-2 agonists often have
a sedating effect, and are commonly used as anesthesia-enhancers in
surgery, as well as in treatment of drug or alcohol dependence. Many
important psychiatric drugs exert strong effects on norepinephrine
systems in the brain, resulting in side-effects that may be helpful or
* 1 Structure
* 2 Biochemical mechanisms
* 2.2 Degradation
* 3 Functions
* 3.1 Cellular effects
* 3.1.1 Storage, release, and reuptake
Sympathetic nervous system
Sympathetic nervous system
* 3.3 Central nervous system
* 4 Pharmacology
* 4.1 Sympathomimetic and sympatholytic drugs
* 4.2 Beta blockers
* 4.3 Alpha blockers
* 4.4 Alpha-2 agonists
* 4.5 Stimulants and antidepressants
* 5 Diseases and disorders
* 5.1 Sympathetic hyperactivation
* 5.3 Stress
* 5.4 ADHD
* 5.5 Autonomic failure
* 6 Comparative biology and evolution
* 7 History
* 8 References
Norepinephrine is a catecholamine and a phenethylamine . Its
structure differs from that of epinephrine only in that epinephrine
has a methyl group attached to its nitrogen, whereas the methyl group
is replaced by a hydrogen atom in norepinephrine. The prefix nor- is
derived as an abbreviation of the word "normal", used to indicate a
Norepinephrine structure Epinephrine
structure Catechol structure
Biosynthetic pathways for catecholamines and trace amines in the
human brain L-
3-Methoxytyramine AADC AADC AADC primary
pathway PNMT PNMT PNMT PNMT AAAH AAAH brain
COMT DBH DBH
Norepinephrine is synthesized from
dopamine in the human body by the dopamine β-hydroxylase (DBH) enzyme
Norepinephrine is synthesized from the amino acid tyrosine by a
series of enzymatic steps in the adrenal medulla and postganglionic
neurons of the sympathetic nervous system . While the conversion of
tyrosine to dopamine occurs predominantly in the cytoplasm, the
conversion of dopamine to norepinephrine by dopamine β-monooxygenase
occurs predominantly inside neurotransmitter vesicles . The metabolic
Thus the direct precursor of norepinephrine is dopamine , which is
synthesized indirectly from the essential amino acid phenylalanine or
the non-essential amino acid tyrosine . These amino acids are found
in nearly every protein and, as such, are provided by ingestion of
protein-containing food, with tyrosine being the most common.
Phenylalanine is converted into tyrosine by the enzyme phenylalanine
hydroxylase , with molecular oxygen (O2) and tetrahydrobiopterin as
Tyrosine is converted into
L-DOPA by the enzyme tyrosine
hydroxylase , with tetrahydrobiopterin , O2, and probably ferrous iron
(Fe2+) as cofactors.
L-DOPA is converted into dopamine by the enzyme
aromatic L-amino acid decarboxylase (also known as DOPA
decarboxylase), with pyridoxal phosphate as a cofactor.
then converted into norepinephrine by the enzyme dopamine
β-monooxygenase (formerly known as dopamine β-hydroxylase), with O2
and ascorbic acid as cofactors.
Norepinephrine itself can further be converted into epinephrine by
the enzyme phenylethanolamine N-methyltransferase with
S-adenosyl-L-methionine as cofactor.
In mammals, norepinephrine is rapidly degraded to various metabolites
. The initial step in the breakdown can be catalyzed by either of the
enzymes monoamine oxidase (mainly monoamine oxidase A ) or
From there the breakdown can proceed by a variety of pathways. The
principal end products are either
Vanillylmandelic acid or a
conjugated form of MHPG , both of which are thought to be biologically
inactive and are excreted in the urine. Norepinephrine
degradation. Metabolizing enzymes are shown in boxes.
Adrenergic receptors in the mammal brain and body
Increase IP3 and calcium by
activating phospholipase C .
Decrease cAMP by
inhibiting adenylate cyclase .
Increase cAMP by
activating adenylate cyclase .
Like many other biologically active substances, norepinephrine exerts
its effects by binding to and activating receptors located on the
surface of cells. Two broad families of norepinephrine receptors have
been identified, known as alpha and beta adrenergic receptors. Alpha
receptors are divided into subtypes α1 and α2 ; beta receptors into
subtypes β1 , β2 , and β3 . All of these function as G
protein-coupled receptors , meaning that they exert their effects via
a complex second messenger system . Alpha-2 receptors usually have
inhibitory effects, but many are located pre-synaptically (i.e., on
the surface of the cells that release norepinephrine), so the net
effect of alpha-2 activation is often a decrease in the amount of
norepinephrine released. Alpha-1 receptors and all three types of
beta receptors usually have excitatory effects.
Storage, Release, And Reuptake
Norepinephrine (labeled "noradrenaline" in this drawing)
processing in a synapse. After release norepinephrine can either be
taken up again by the presynaptic terminal, or broken down by enzymes.
Inside the brain norepinephrine functions as a neurotransmitter , and
is controlled by a set of mechanisms common to all monoamine
neurotransmitters . After synthesis, norepinephrine is transported
from the cytosol into synaptic vesicles by the vesicular monoamine
Norepinephrine is stored in these vesicles until
it is ejected into the synaptic cleft , typically after an action
potential causes the vesicles to release their contents directly into
the synaptic cleft through a process called exocytosis .
Once in the synapse, norepinephrine binds to and activates receptors.
After an action potential, the norepinephrine molecules quickly become
unbound from their receptors. They are then absorbed back into the
presynaptic cell, via reuptake mediated primarily by the
norepinephrine transporter (NET). Once back in the cytosol,
norepinephrine can either be broken down by monoamine oxidase or
repackaged into vesicles by VMAT, making it available for future
SYMPATHETIC NERVOUS SYSTEM
Sympathetic nervous system
Sympathetic nervous system Schema of the
sympathetic nervous system, showing the sympathetic ganglia and the
parts of the body to which they connect.
Norepinephrine is the main neurotransmitter used by the sympathetic
nervous system, which consists of about two dozen sympathetic chain
ganglia located next to the spinal cord, plus a set of prevertebral
ganglia located in the chest and abdomen. These sympathetic ganglia
are connected to numerous organs, including the eyes, salivary glands,
heart, lungs, liver, gallbladder, stomach, intestines, kidneys,
urinary bladder, reproductive organs, muscles, skin, and adrenal
glands. Sympathetic activation of the adrenal glands causes the part
called the adrenal medulla to release norepinephrine into the
bloodstream, from which, functioning as a hormone , it gains further
access to a wide variety of tissues.
Broadly speaking, the effect of norepinephrine on each target organ
is to modify its state in a way that makes it more conducive to active
body movement, often at a cost of increased energy use and increased
wear and tear. This can be contrasted with the acetylcholine
-mediated effects of the parasympathetic nervous system , which
modifies most of the same organs into a state more conducive to rest,
recovery, and digestion of food, and usually less costly in terms of
The sympathetic effects of norepinephrine include:
* In the eyes, an increase in production of tears, making the eyes
more moist., and pupil dilation through contraction of the iris
* In the heart, an increase in the amount of blood pumped.
* In brown adipose tissue , an increase in calories burned to
generate body heat.
* Multiple effects on the immune system . The sympathetic nervous
system is the primary path of interaction between the immune system
and the brain, and several components receive sympathetic inputs,
including the thymus , spleen , and lymph nodes . However the effects
are complex, with some immune processes activated while others are
* In the arteries , constriction of blood vessels, causing an
increase in blood pressure.
* In the kidneys , release of renin and retention of sodium in the
* In the liver , an increase in production of glucose , either by
glycogenolysis after a meal or by gluconeogenesis when food has not
recently been consumed.
Glucose is the body's main energy source in
* In the pancreas , increased release of glucagon , a hormone whose
main effect is to increase the production of glucose by the liver.
* In skeletal muscles, an increase in glucose uptake.
* In adipose tissue (i. e., fat cells), an increase in lipolysis ,
that is, conversion of fat to substances that can be used directly as
energy sources by muscles and other tissues.
* In the stomach and intestines, a reduction in digestive activity.
This results from a generally inhibitory effect of norepinephrine on
the enteric nervous system , causing decreases in gastrointestinal
mobility, blood flow, and secretion of digestive substances.
CENTRAL NERVOUS SYSTEM
Brain areas containing noradrenergic neurons.
The noradrenergic neurons in the brain form a neurotransmitter system
, that, when activated, exerts effects on large areas of the brain.
The effects are manifested in alertness, arousal , and readiness for
Noradrenergic neurons (i.e., neurons whose primary neurotransmitter
is norepinephrine) are comparatively few in number, and their cell
bodies are confined to a few relatively small brain areas, but they
send projections to many other brain areas and exert powerful effects
on their targets. These noradrenergic cell groups were first mapped in
1964 by Annica Dahlström and Kjell Fuxe, who assigned them labels
starting with the letter "A" (for "aminergic"). In their scheme,
areas A1 through A7 contain the neurotransmitter norepinephrine (A8
through A14 contain dopamine ).
Noradrenergic cell group A1 is located
in the caudal ventrolateral part of the medulla, and plays a role in
the control of body fluid metabolism.
Noradrenergic cell group A2 is
located in a brainstem area called the solitary nucleus ; these cells
have been implicated in a variety of responses, including control of
food intake and responses to stress. Cell groups A5 and A7 project
mainly to the spinal cord.
The most important source of norepinephrine in the brain is the locus
coeruleus , which contains noradrenergic cell group A6 and adjoins
cell group A4 . The locus coeruleus is quite small in absolute
terms—in primates it is estimated to contain around 15,000 neurons,
less than one millionth of the neurons in the brain—but it sends
projections to every major part of the brain and also to the spinal
The level of activity in the locus coeruleus correlates broadly with
vigilance and speed of reaction. LC activity is low during sleep and
drops to virtually nothing during the REM (dreaming) state. It runs
at a baseline level during wakefulness, but increases temporarily when
a person is presented with any sort of stimulus that draws attention.
Unpleasant stimuli such as pain, difficulty breathing, bladder
distension, heat or cold generate larger increases. Extremely
unpleasant states such as intense fear or intense pain are associated
with very high levels of LC activity.
Norepinephrine released by the locus coeruleus affects brain function
in a number of ways. It enhances processing of sensory inputs,
enhances attention, enhances formation and retrieval of both long term
and working memory, and enhances the ability of the brain to respond
to inputs by changing the activity pattern in the prefrontal cortex
and other areas. The control of arousal level is strong enough that
drug-induced suppression of the LC has a powerful sedating effect.
There is great similarity between situations that activate the locus
coeruleus in the brain and situations that activate the sympathetic
nervous system in the periphery: the LC essentially mobilizes the
brain for action while the sympathetic system mobilizes the body. It
has been argued that this similarity arises because both are to a
large degree controlled by the same brain structures, particularly a
part of the brainstem called the nucleus gigantocellularis .
A large number of important drugs exert their effects by interacting
with norepinephrine systems in the brain or body. Their uses include
treatment of cardiovascular problems, shock, and a variety of
SYMPATHOMIMETIC AND SYMPATHOLYTIC DRUGS
Sympathomimetic drugs mimic or enhance at least some of the effects
of norepinephrine released by the sympathetic nervous system;
sympatholytic drugs, in contrast, block at least some of the effects.
Both of these are large groups with diverse uses, depending on exactly
which effects are enhanced or blocked.
Norepinephrine itself is
classified as a sympathomimetic drug: its effects when given by
intravenous injection of increasing heart rate and force and
constricting blood vessels make it very useful for treating medical
emergencies that involve critically low blood pressure.
These are drugs that block the effects of beta noradrenergic
receptors while having little or no effect on alpha receptors. They
are sometimes used to treat high blood pressure , atrial fibrillation
and congestive heart failure , but recent reviews have concluded that
other types of drugs are usually superior for those purposes. Beta
blockers may be a viable choice for other cardiovascular conditions,
though, including angina and
Marfan syndrome . They are also widely
used to treat glaucoma , either in pill form or in eyedrops. Because
of their effects in reducing anxiety symptoms and tremor, they have
sometimes been used by entertainers, public speakers and athletes to
reduce performance anxiety , although they are not medically approved
for that purpose and are banned by the International Olympic Committee
However, the usefulness of beta blockers is limited by a range of
serious side effects, including slowing of heart rate, a drop in blood
pressure, asthma, and reactive hypoglycemia . The negative effects
can be particularly severe in people who suffer from diabetes .
These are drugs that block the effects of noradrenergic alpha
receptors while having little or no effect on beta receptors. Drugs
belonging to this group can have very different effects, however,
depending on whether they primarily block alpha-1 receptors, alpha-2
receptors, or both. Alpha-2 receptors, as described elsewhere in this
article, are frequently located on norepinephrine-releasing neurons
themselves and have inhibitory effects on them; consequently blockage
of alpha-2 receptors usually results in an increase in norepinephrine
release. Alpha-1 receptors are usually located on target cells and
have excitatory effects on them; consequently blockage of alpha-1
receptors usually results in blocking some of the effects of
norepinephrine. Drugs such as phentolamine that act on both types of
receptors can produce a complex combination of both effects. In most
cases when the term "alpha blocker" is used without qualification, it
refers to a selective alpha-1 antagonist.
Selective alpha-1 blockers have a variety of uses. Because one of
their effects is to relax the muscles in the neck of the bladder, they
are often used to treat benign prostatic hyperplasia , and to help
with the expulsion of bladder stones . Their effects on the central
nervous system make them useful for treating generalized anxiety
disorder , panic disorder , and posttraumatic stress disorder . They
may, however, have significant side-effects, including a drop in blood
Some antidepressants function partly as selective alpha-2 blockers ,
but the best-known drug in that class is yohimbine , which is
extracted from the bark of the African yohimbe tree.
as a male potency enhancer , but its usefulness for that purpose is
limited by serious side-effects including anxiety and insomnia.
Overdoses can cause a dangerous increase in blood pressure. Yohimbine
is banned in many countries, but in the United States, because it is
extracted from a plant rather than chemically synthesized, it is sold
over the counter as a nutritional supplement .
These are drugs that activate alpha-2 receptors or enhance their
effects. Because alpha-2 receptors are inhibitory and many are located
presynaptically on norepinephrine-releasing cells, the net effect of
these drugs is usually to reduce the amount of norepinephrine
released. Drugs in this group that are capable of entering the brain
often have strong sedating effects, due to their inhibitory effects on
the locus coeruleus .
Clonidine , for example, is used for the
treatment of anxiety disorders and insomnia, and also as a sedative
premedication for patients about to undergo surgery.
another drug in this group, is also a powerful sedative and is often
used in combination with ketamine as a general anaesthetic for
veterinary surgery —in the United States it has not been approved
for use in humans.
STIMULANTS AND ANTIDEPRESSANTS
Stimulant § Mechanisms of action , and
These are drugs whose primary effects are thought to be mediated by
different neurotransmitter systems (dopamine for stimulants ,
serotonin for antidepressants ), but many also increase levels of
norepinephrine in the brain.
Amphetamine , for example, is a stimulant
that increases release of norepinephrine as well as dopamine.
Monoamine oxidase inhibitors are antidepressants that inhibit the
metabolic degradation of norepinephrine as well as serotonin. In some
cases it is difficult to distinguish the norepinephrine-mediated
effects from the effects related to other neurotransmitters.
DISEASES AND DISORDERS
A number of important medical problems involve dysfunction of the
norepinephrine system in the brain or body.
Hyperactivation of the sympathetic nervous system is not a recognized
condition in itself, but it is a component of a number of conditions,
as well as a possible consequence of taking sympathomimetic drugs . It
causes a distinctive set of symptoms including aches and pains, rapid
heartbeat, elevated blood pressure, sweating, palpitations, anxiety,
headache, paleness, and a drop in blood glucose. If sympathetic
activity is elevated for an extended time, it can cause weight loss
and other stress-related body changes.
The list of conditions that can cause sympathetic hyperactivation
includes severe brain injury, spinal cord damage, heart failure,
high blood pressure, kidney disease, and various types of stress.
A pheochromocytoma is a rarely occurring tumor of the adrenal medulla
, caused either by genetic factors or certain types of cancer. The
consequence is a massive increase in the amount of norepinephrine and
epinephrine released into the bloodstream. The most obvious symptoms
are those of sympathetic hyperactivation, including particularly a
rise in blood pressure that can reach fatal levels. The most effective
treatment is surgical removal of the tumor.
Stress , to a physiologist, means any situation that threatens the
continued stability of the body and its functions. Stress affects a
wide variety of body systems: the two most consistently activated are
the hypothalamic-pituitary-adrenal axis and the norepinephrine system,
including both the sympathetic nervous system and the locus coeruleus
-centered system in the brain. Stressors of many types evoke
increases in noradrenergic activity, which mobilizes the brain and
body to meet the threat. Chronic stress, if continued for a long
time, can damage many parts of the body. A significant part of the
damage is due to the effects of sustained norepinephrine release,
because of norepinephrine's general function of directing resources
away from maintenance, regeneration, and reproduction, and toward
systems that are required for active movement. The consequences can
include slowing of growth (in children), sleeplessness, loss of
libido, gastrointestinal problems, impaired disease resistance, slower
rates of injury healing, depression, and increased vulnerability to
Attention deficit hyperactivity disorder
Attention deficit hyperactivity disorder is a psychiatric condition
involving problems with attention, hyperactivity, and impulsiveness.
It is most commonly treated using stimulant drugs such as
methylphenidate (Ritalin), whose primary effect is to increase
dopamine levels in the brain, but drugs in this group also generally
increase brain levels of norepinephrine, and it has been difficult to
determine whether these actions are involved in their clinical value.
Also there is substantial evidence that many people with ADHD show
"biomarkers" involving altered norepinephrine processing. Several
drugs whose primary effects are on norepinephrine, including
guanfacine , clonidine , and atomoxetine , have been tried as
treatments for ADHD, and found to have effects comparable to those of
Several conditions, including Parkinson\'s disease , diabetes and
so-called pure autonomic failure , can cause a loss of
norepinephrine-secreting neurons in the sympathetic nervous system.
The symptoms are widespread, the most serious being a reduction in
heart rate and an extreme drop in resting blood pressure, making it
impossible for severely affected people to stand for more than a few
seconds without fainting. Treatment can involve dietary changes or
COMPARATIVE BIOLOGY AND EVOLUTION
Chemical structure of octopamine , which serves as the homologue
of norepinephrine in many invertebrate species
Norepinephrine has been reported to exist in a wide variety of animal
species, including protozoa , placozoa and cnidaria (jellyfish and
related species), but not in ctenophores (comb jellies), whose
nervous systems differ greatly from those of other animals. It is
generally present in deuterostomes (vertebrates, etc.), but in
protostomes (arthropods, molluscs, flatworms, nematodes, annelids,
etc.) it is replaced by octopamine , a closely related chemical with a
closely related synthesis pathway. In insects, octopamine has
alerting and activating functions that correspond (at least roughly)
with the functions of norepinephrine in vertebrates. It has been
argued that octopamine evolved to replace norepinephrine rather than
vice versa; however, the nervous system of amphioxus (a primitive
chordate) has been reported to contain octopamine but not
norepinephrine, which presents difficulties for that hypothesis.
History of catecholamine research
Early in the twentieth century Walter Cannon , who had popularized
the idea of a sympathoadrenal system preparing the body for fight and
flight , and his colleague
Arturo Rosenblueth developed a theory of
two sympathins, sympathin E (excitatory) and sympathin I (inhibitory),
responsible for these actions. The Belgian pharmacologist Zénon Bacq
as well as Canadian and US-American pharmacologists between 1934 and
1938 suggested that noradrenaline might be a sympathetic transmitter.
In 1939, Hermann Blaschko and Peter Holtz independently identified the
biosynthetic mechanism for norepinephrine in the vertebrate body. In
Ulf von Euler published the first of a series of papers that
established the role of norepinephrine as a neurotransmitter. He
demonstrated the presence of norepinephrine in sympathetically
innervated tissues and brain, and adduced evidence that it is the
sympathin of Cannon and Rosenblueth.
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AMINO ACID -DERIVED
* MAJOR EXCITATORY/INHIBITORY SYSTEMS: Glutamate system:
Aspartic acid (aspartate)
Glutamic acid (glutamate)
Serine ; GABA system: GABA
* GHB ;
Glycine system: α-Alanine
Taurine ; GHB system: GHB
* T-HCA (GHC)
* BIOGENIC AMINES: Monoamines: 6-OHM
* NAS (normelatonin)
Serotonin (5-HT) ; Trace amines:
Tyramine ; Others:
* NEUROPEPTIDES: See here instead.
* ENDOCANNABINOIDS: 2-AG
* 2-AGE (noladin ether)
* NEUROSTEROIDS: See here instead.
* Cholinergic system:
Carbon monoxide (CO)
Hydrogen sulfide (H2S)
Nitric oxide (NO) ; Candidates:
Carbonyl sulfide (COS)
Nitrous oxide (N2O)
Sulfur dioxide (SO2)
* Adrenal cortex
* activin and inhibin
* relaxin (pregnancy)
* pancreatic polypeptide
* peptide YY
Insulin-like growth factor
Insulin-like growth factor
* JGA (renin )
* peritubular cells
Adrenergic receptor modulators
Corbadrine Desglymidodrine Dexisometheptene
antipsychotics (e.g., clozapine , olanzapine , quetiapine ,
Doxazosin Ergolines (e.g.,
ergotamine , dihydroergotamine , lisuride , terguride )
Trazodone Tetracyclic antidepressants (e.g., amoxapine , maprotiline
, mianserin ) Tricyclic antidepressants (e.g., amitriptyline ,
clomipramine , doxepin , imipramine , trimipramine )
Typical antipsychotics (e.g., chlorpromazine , fluphenazine , loxapine
, thioridazine )
L-DOPA (levodopa) L-
antipsychotics (e.g., asenapine , clozapine , lurasidone ,
paliperidone , quetiapine , risperidone , zotepine ) Azapirones (e.g.,
buspirone , tandospirone )
antipsychotics (e.g., chlorpromazine , fluphenazine , loxapine ,
L-DOPA (levodopa) L-
* SEE ALSO: Receptor/signaling modulators
* Monoamine reuptake inhibitors
* Monoamine releasing agents
* Monoamine metabolism modulators
* Monoamine neurotoxins
Human trace amine-associated receptor ligands
* Classical monoamine neurotransmitters
* Trace amines
†References for all endogenous human
TAAR1 ligands are provided
at List of trace amines
‡References for synthetic
TAAR1 agonists can be found at
in the associated compound articles. For
TAAR5 agonists and
inverse agonists, see TAAR for references.
SEE ALSO: Receptor/signaling modulators
* α-Methylphenethylamine (amphetamine)
Others: BOH * DMPEA
Stimulants: 2-FA * 2-FMA
* L -Norpseudoephedrine
Entactogens: 4-FA * 4-FMA
Others: 3,4-DCA *
Selegiline (also D -Deprenyl )
* Stimulants: 3-FMC
Entactogens: 3,4-DMMC * 3-MMC
* Entactogens: 4-CAB
* Stimulants: α-PBP
(and close relatives)
* D -DOPA (Dextrodopa)
* L -DOPA (Levodopa)
* L -DOPS (Droxidopa)
* L -
* L -
Lysergic acid amide
Lysergic acid 2-butyl amide
Lysergic acid 2,4-dimethylazetidide
Lysergic acid 2,4-dimethylazetidide
Lysergic acid diethylamide
Lysergic acid diethylamide
* GND : 4171995-5