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A metabolite of synephrine, Octopamine is a stimulant compound that is also thought to have minor fat burning effects. Banned by WADA due to its stimulatory properties, the direct fat burning claims may not be relevant and are effectively untested in humans.

Our evidence-based analysis on octopamine features 66 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
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Research Breakdown on Octopamine

1Sources and Composition

1.1Sources and Structure

Octopamine (β,4-dihydroxyphenethylamine) is a trace amine found endogenously in the human brain where it interacts with signalling of catecholamines; it is structurally similar to synephrine and tyramine, being a metabolite of the latter (via dopamine β-hydroxylase[2]) and substrate for the synthesis of the former (via phenethanolamine N-methyltransferase[3]) while being perhaps the closest in structure to noradrenaline.

The common name octopamine originated from the source of its discovery in 1940, from the salivary gland of the octopus (octopus vulgaris; cited indirectly as the original source is not located online[4]).

Octopamine and the trace amine tyramine are both known to be predominant neuromodulators in invertebrates where their signalling pathway is coupled to adenylyl cyclase (to produce cAMP)[5] and parallels the human catecholamine signalling system;[6][7] however, these receptors are not expressed in humans and octopamine seems to interact with the adrenergic receptors themselves or trace amine receptors.

Octopamine is one of the final products of L-tyrosine metabolism in the human, and is used as an intermediate from which the body can make synephrine from. It has a major role in invertebrates which cannot be extended to humans (similar to ecdysteroids)

Dietary supplements that are said to contain bitter orange (Citrus aurantium) may contain synephrine, octopamine, and tyramine[8] with synephrine being the most prominent inclusion and octopamine in the range of 140-900µg/g (although it is usually 1.0-1.3% the content of synephrine and comparable to the tyramine content).[9][10]

Citrus aurantium contains a variety of biogenic amines, all with structural similarity:

  • L-tyrosine is the parent amino acid from which biogenic amines (not of the phenylethylamine class) are derived from

  • Decarboxylated L-tyrosine is tyramine

  • A methylation of the amine group of tyramine leads to N-methyltyramine, and another methylation leads to the production of hordenine

  • If tyramine is hydroxylated the octopamine is the result, whereas if N-methyltyramine is hydroxylated then synephrine is the rest

And other natural sources which contain octopamine include:

  • Garlic peel which contains N-trans-coumaroyloctopamine and N-trans-feruloyloctopamine,[11] two known tyrosinase inhibitors (IC50 values less than 10µM[12])

  • Acorus Tatarinowii (containing N-trans-coumaroyloctopamine and N-trans-feruloyloctopamine[13])

Octopamine is found in the bitter orange similar to many biogenic amines related to L-tyrosine that are used as dietary supplements, this includes synephrine and hordenine

Octopamine in general can occur in one of three isomers preceded with meta (m), ortho (o), or para (p) to produce isomer names such as p-octopamine; a similar naming system to synephrine. Additionally, both the R form of (-)- and the S form of (+)- exist as enantiomers leading to six possible variants of octopamine:[14][15]

  • (-)-p-octopamine

  • (+)-p-octopamine

  • (-)-m-octopamine

  • (+)-m-octopamine

  • (-)-o-octopamine

  • (+)- o-octopamine

An italicized l or d are sometimes used for designating enantiomers and correspond with R and S respectively, meaning that R-p-octopamine, (-)-p-octopamine, and D-p-octopamine are synonymous. Further synonyms include norsynephrine (referring to p-octopamine) and norfenefrine (referring to m-octopamine).

P-octopamine tends to be synthesized endogenously from dietary L-tyrosine (indirectly) and is thought to only endogenously exist in the R enantiomer, suggesting that R-p-octopamine is the major naturally occurring form in humans.[14] Some m-octopamine has been detected in human nervous tissues and brain[16] despite not occurring in plants,[17] and o-octopamine is seen as fully synthetic as it has not been detected in nature.

Octopamine could exist in one of six differing forms, due to the position of the hydroxyl group on the benzene ring (giving rise to isomers) or the orientation of the hydroxyl group in the amine sidechain (giving rise to enantiomers of the aforementioned isomers)

2Molecular Targets

2.1Trace Amine Receptors

The trace amine receptors (TA receptors or TAARs) are intracellular receptors that induce cAMP accumulation upon activation, showing structural and functional parallels with β-adrenergic and rhodopsin receptor superfamily;[18] ligands to these receptors include octopamine and other trace amines such as phenylethylamine (PEA) and tyramine but also many hallucinogenic and enactogenic drugs.[19][20]



Due to urinary elimination of octopamine and its metabolites to be comparable with oral (8mg on an empty stomach) and intravenous administration of the same dose, it is assumed that oral bioavailability in the human is complete.[21] Despite the near perfect absorption, it has been noted to be heavily conjugated in the intestines and liver[21] so that 0.58% of the oral dose is considered 'free' octopamine (after accounting for metabolism via MAO and conjugation).[22]

3.2Transportation in Serum

Independent of supplementation, baseline octopamine levels in serum have been noted to be in the low nanomolar range including 4.28+/-0.28ng/mL in otherwise healthy aged (60) controls.[23] It can be found in platelets in concentrations paralleling adrenaline and noradrenaline.[24]

Following supplementation of 8mg p-octopamine, the halflife appears to be biexponential[22][8] at 76 and 175 minutes,[22] thought to possibly be explained by conjugates being hydrolyzed back into free p-octopamine.[14]

3.3Neurological Distribution

Similar to phenylethylamine and other trace amines, octopamine (both p and m enantiomers) appears to be endogenously expressed in brain regions subserving autonomic function where TA receptors are also expressed.[16]


Octopamine is metabolized by both monoamine oxidase (MAO) enzymes type A and B, similar to phenylethylamine[25][26] but may also be metabolized by Semicarbazide-sensitive amine oxidase (SSAO or Amine Oxidase).[27] When subject to either of these enzymes, octopamine is deaminated into the metabolite known as p-hydroxymandelic acid (if p-octopamine) or m-hydroxymandelic acid (if m-octopamine).[22][21]

It is possible for octopamine to be conjugated, and at least with m-octopamine the degree of unconjugated octopamine appears to be higher following intravenous administration (10.5%) relative to oral (0.58%) suggesting a high degree of conjugation during first pass metabolism.[21] It is possible that this hinders the efficacy of octopamine somewhat, as its usage for the treatment of hypotensive disorders has been known to have reduced potency with the oral route relative to intravenous.[22]

Administration of MAO inhibitors to the rat fed tyramine (known to produce urinary levels of octopamine) can increase urinary free octopamine 10-fold, secondary to reducing oxidative metabolism to hydroxymandelic acids.[28]


Hydroxymandelic acid metabolites account for two thirds of orally ingested octopamine in man, and are eliminated via the urine.[22][21] Other metabolites include either unchanged octopamine, the metabolite hydroxyphenolglycol,[28] or either of the aforementioned two as well as octopamine conjugated via first pass metabolism.[22][21][28] Up to 93% of ingested octopamine is elimianted via the urinary route within 24 hours[22] and peaks in the urine following four hours after oral administration (drug testing case studies).[8]

When a high dose of synephrine is given to participants orally, no octopamine is produced endogenously[8][29] suggesting that the synthesis of synephrine from octopamine via N-methylation[30] occurs in reverse (demethylation) to a rate comparable to oxidative degradation of octopamine into hydroxymandelic acid resulting in no significant accumulation of octopamine.[14] The major urinary metabolite of synephrine is also hydroxymandelic acid of the corresponding enantiomer.[31]

While octopamine is an intermediate of synephrine metabolism and should transiently arise with synephrine supplementation, it is thought that rapid metabolism of octopamine produced in this manner prevents increases in urinary octopamine (important as while octopamine is banned by WADA, synephrine is not)


4.1Adrenergic Neurotransmission

In invertebrates, the role of the octopamine/tyramine signalling pathways parallels that of catecholamine (adrenaline and dopamine) in humans[6][7] with octopamine in humans thought to be only indirectly implicated in adrenergic neurotransmission as a TA receptor ligand.

A large amount of information on octopamine as it relates to adrenergic signalling, if conducted in invertebrates, cannot reliably be extended to humans due to species differences. This includes in vitro studies using cells or receptors isolated from insects rather than mammalian cells

Octopamine has been noted to be an agonist of human β1-receptors (EC50 of 3,129+/-461nM[32]) and an agonist of β3 (adipocytes[33]), although it appears to have no effects on β2 receptors (transfected HEK293) up to a concentration of 6.7µM while allosterically inhibiting other agonists (isoprenaline).

At the level of the α-adrenergic receptor, m-octopamine appears to be an agonist that is said to be one hundreth the potency of noradrenaline overall[34] which is thought to be due less to its potency on α2-adrenergic receptors (around 150-fold less poteny[15]) and more due to its actions on α1-adrenergic receptors as they are only 6-fold less potent.[15] M-octopamine is the most potent of the octopamine isomers on these receptors with p-octopamine being more than 10-fold weaker than m-octopamine[34][15] and o-octopamine being the weakest[15] while in regards to the enantiomers the (-)- formation is more effective than the (+)- formation.[15]

When assessing the α2A-adrenergic receptor in particular, a racemic mixture of m-octopamine was noted to inhibit cAMP at 10µM secondary to this receptor whereas the least potent form of (+)-p-octopamine failed to have any effect at 100µM.[35]

Octopamine appears to be a ligand for the adrenergic receptors including both the alpha and beta classes, although the concentrations needed to target the alpha receptors seem to be significantly higher than those required to activate the beta receptors. Although this would normally suggest selectivity, the concentrations required for octopamine to act on these receptors (except perhaps β3) seems higher than oral supplementation can feasibly produce

4.2Dopaminergic Neurotransmission

Octopamine has been noted to interact with dopamine receptors, binding to the same spot on the D1 receptor as the research antagonist SCH-23390[36][37] with no apparent affinity for the D2 receptor.[36] At least in stomach tissue, the antagonism of the D1 receptor occurred at 1μM and could fully ablate dopamine (agonist) when it was at the EC50 value or less[38] and has been noted to be effective in the brains of mice at the intraperitoneal (injection) dose of 10mg/kg.[37]

Elsewhere and in jejunal (intestinal) tissue of the rabbit, octopamine has demonstrated agonistic properties on the D1 receptor in a manner blocked by SCH-23390.[39] The reason for the difference noted in intestinal tissue and neural tissue is not clear.

Although there is no current evidence in humans, it appears that octopamine has a role in inhibiting the activity of the D1 receptor (thereby changing dopamine signalling towards other receptors such as D2) and this occurs at a concentration which is not astoundingly high

The human dopamine transporter (DAT) in HEK293 cells appears to have affinity for dl-octopamine, which interacted with a KD of 220μM which was weaker than p-tyramine (22μM) and D-amphetamine (5.5μM)[40] with its efficacy positively correlated with the sodium content of the medium (DAT being a sodium chloride dependent transporter)[41][40] although not dependent on it.[42] The reduced potency of octopamine relative to tyramine is thought to be due to hydroxylation on the β-carbon on the sidechain, which is known to reduce affinity for the DAT of similarly structured compounds.[40]

Octopamine is known to have affinity for the dopamine transporter, perhaps as a substrate, but when tested in vitro it seems to have fairly low affinity (relative to the concentration of it expected in the brain). The interactions of octopamine and the DAT in vitro need further research

4.3Headaches and Blood Flow

Trace amine metabolism is known to be perturbed in persons who suffer from migraines,[43] and octopamine has been measured in platelets to be significantly higher in persons with migraines without accompanying auras[44] whereas the opposite occurring in migraine with aura where synephrine was higher and octopamine unaltered.[44] Platelet levels of octopamine have also been noted to be higher in persons with primary headache[45] although elsewhere in persons with chronic migraine octopamine was unaltered despite increases in catecholamines and tyramine in those with chronic migraine.[46]

Other instances of migraine, such as those that may occur alongside eating disorders (high prevalence rate at times exceeding 75%[47]) have noted comparable levels of octopamine in persons with eating disorders relative to control subjects[48][47] although it may be slightly reduced in anorexia nervosa relative to bulimia nervosa (which had elevated tyramine relative to anorexia).[48]

Chronic tension-type headache (CTTH), which differs from chornic migraines as they do not possess all the acute side-effects of migraines (photophobia, osmophobia, phonophobia, nausea[49]), do not appear to have abnormalities in the overall L-tyrosine metabolic pathway like chronic migraines do.[46]

In general, migraine may be associated with abnormalities in L-tyrosine metabolism which implicate the catecholamines (noradrenaline and dopamine) as well as trace amines such as octopamine and tyramine. These abnormalities do not extend to all forms of migraine, and a role for octopamine supplementation is not currently known in this regard

5Fat Mass and Obesity


Octopamine has been noted to be able to inhibit glucose uptake into an adipocyte (100μM) acutely via activation of the β3 adrenoceptor[50] although there was an additional enhancement of glucose uptake via a different mechanism;[50] octopamine can be metabolized in fat cells by monoamine oxidase (MAO[51]) or semicarbazide-sensitive amine oxidase (SSAO[52]) to form an oxidative byproduct creatine hydrogen peroxide (H2O2)[50] which itself is thought to activate AMPK.[53] This pathway also extends to tyramine which has similar metabolism as octopamine, and the glucose uptake enhanced with increased oxidation.[54]

Mixed effects on glucose uptake into fat cells due to two divergent mechanisms, and practical relevance of this information towards supplemental octopamine is unknown

5.2Fat Oxidation

When incubated in fat cells taken from obese patients, m-octopamine (10µM) increases lipolysis secondary to activating the α1-adrenergic receptor with a similar potency to a similarly high concentraiton of noradrenaline.[55] This particular subset of the alpha receptors (in contrast to α2 receptors which are antilipolytic via cAMP inhibition[56]) increase calcium mobilization and PKC activation resulting in glycerol release.[57][58] Despite previous evidence noting activation of α2 receptors in neurons with octopamine at high concentrations,[15] this was not noted with p-octopamine which failed up to 100µM in neurons to activate this subset[35] and the failure replicated in adipocytes.[59][50] 

When using an isomer of octopamine that exerts lipolytic effects via β3 agonism and antilipolytic effects via α2 agonism, the former appears to be more significant resulting in a net lipolytic effect;[59] ablating the β3 receptors results in only a weak lipogenic effect,[59] possibly due to still acting in a lipolytic manner via α1 adrenoceptors.[55]

Octopamine activates both α1 adrenergic receptors (causes lipolysis) and α2 adrenergic receptors (inhibits lipolysis), although it seems that p-octopamine is commonly used as a fat loss supplement since this particular isomer does not activate the latter subset of adrenergic receptors

P-octopamine interacts with the β-adrenergic receptors in adipocytes, although it seems to be able to active lipolysis to a significantly larger degree in rat and hamster cells relative to human cells[33] thought to be due to a significantly higher percentage of β3-adrenoceptors (present in brown fat, but limited in white fat in humans[60]). P-octopamine appears to have only 2-fold less potency than noradrenaline on β3-adrenoceptors, while bearing 200-fold less affinity on cells expressed β1 and β2.[33]

Octopamine is a full agonist of the β3 receptor with weak affinity for the other two receptor subtypes, suggesting that following oral supplementation it would be a selective β3 receptor activator. While this receptor mediates fat loss effects of octopamine, it is not known to be expressed to a high degree in human white adipose tissue (being expressed more in brown adipose tissue and in rodents relative to humans)

6Peripheral Organ Systems


Dopamine appears to stimulate acid secretion from the rat stomach (EC50 of 600nM) in a manner which is antagonized by octopamine at a concentration of 1µM.[38] Dopamine was also antagonized by a selective D1 receptor antagonist (SCH23390[38]) of which octopamine has been noted to parallel in action and binding site.[36]


M-octopamine has been tested for its role in treating mild incontinence in females due to its α-adrenergic agonist properties (a class of drugs used to treat incontinence in females[61]), most studies using the pharmaceutical formulation Nevadral Retard (retard referring to the slow-release encapsulation). This formulation at the dose of 90mg can acutely increase urethral pressure[62] which is thought to persist after six weeks supplementation.[63]

The first study to note benefit was a pilot study using 60mg in slow release tablets for three months noting a 35% response rate in subjects becoming subjectively continent,[64] and later studies have increased the dose up to 30mg thrice daily (90mg total) over a prolonged period of time (variable between 3-24 weeks) in women with mild incontinence which has been noted to show improvements relative to baseline as assessed by a 1-hour pad test.[65] When subject to a double blind study with a similar dosing protocol (15-30mg thrice daily, total daily dose of 45-90mg for six weeks) where a 52% improvement in subjective symptoms and 26% of the subjects reported full continence;[63] while the increase in urethral pressure seen with supplementation (10%) was not significant relative to placebo overall, it was noted to be significant in persons with worse baseline incontinence.[63]

7Longevity and Life Extension


It has been noted in aged rats that, despite no abnormalities seen with catecholamines during old age, that p-octopamine and p-tyramine were both reduced relative to youth[66] hypothesized to be related to lower activity of the L-amino acid decarboxylase enzyme (which mediates the conversion of L-tyrosine into tyramine).

8Other Medical Conditions

8.1Parkinson's Disease

In persons with Parkinson's disease, serum octopamine was lower overall (1.80+/-0.22ng/mL) and particularly those in the early stages of Parkinson's disease (0.65+/-0.16ng/mL) relative to nondiseased controls (4.28+/-0.28ng/mL).[23]

9Safety and Toxicology


While there does not appear to be published data showing adverse effects of octopamine supplementation in humans (2014), this is due to an overall lack of human studies with oral supplementation.[14] 

Up to 90mg of m-octopamine (norfenefrine) has been used for up to 24 weeks with no significant side effects (save for one subject who experienced nausea thought to be related to supplementation)[65] and the same dose used in a six week double blind study failed to find any significant differences in side-effects relative to placebo;[63] it should be noted that both studies used the formulation known as Nevadral Retard which is a time release formulation.


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