Coleus Forskohlii

Last Updated: November 17, 2022

Coleus forskohlii is an herb used in traditional medicine that may boost testosterone and induce fat loss, particularly in men.

Coleus Forskohlii is most often used for.

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Source and Composition



Coleus Forskohlii of the family Lamiaceae (alternate name of Plectranthus barbatus) is traditionally used in Ayurveda (Ayurvedic medicine) for various cardiovascular, gastrointestinal, and central nervous system ailments.[1] It also has some implications in lung health and urinary health.[2]

Other names of coleus include 'falso boldo' (in brazil[3])



The aerial parts of coleus forskohlii (leafs and stem) include:

  • The forskolin series of related compounds (A,G,H,I,J)and isoforskolin[4][5][6][7] The main forskolin compound used in research has the technical name 7beta-acetoxy-1alpha,6beta,9alpha-trihydroxy-8,13-epoxy-labd-14-en-11-one.[8]
  • The Forskoditerpenoside series (A,C,D,E) of diterpene structures.[9][10]
  • (16S)-Coleon E[3]
  • 4beta,7beta,11-enantioeudesmantriol[10]
  • Rosmarinic acid (leaves)[11]
  • Abietane diterpenoids[12]
  • Chamaecydin[4]
  • Scutellarein as 4′-methyl ether 7-O-glucuronide[3]
  • Luteolin as 7-O-Glucuronide[12]
  • Apigenin as 7-O-glucuronide[12]
  • Acacetin as 7-O-glucuronide[12]
  • Alpha-cedrene[4]
  • Oleanolic Acid[4] and Betulinic acid[4]
  • Beta-sitosterol[4]

Whereas the root portion contains:

  • 14-deoxycoleon U[13]
  • Demethylcryptojapnol[13]
  • Alpha-Amyrin and Alpha-Cedrol[13]
  • Betulinic acid[13]
  • Beta-sitosterol[13]

It is typically used for its active component, Forskolin, which is a direct activator of a cellular intermediate called Adenylate Cyclase.[14] Also called coleonol, Forskolin is found in varying concentrations in different plants of Coleus Forskohlii.[2] It is a yellowish brown powder when supplemented, and has a pleasing aroma yet bitter taste; when supplementing the whole plant the color is more brown in appearance.[2] Forskolin has poor solubility in water but is otherwise quite stable.[15]


Variants and Formulations

Forskolin itself has poor water solubility, and activates 8 out of 9 isoforms of Adenylate Cyclase. This is seen as undesirable by some, as increasing cAMP in other organs aside from the target organ can give rise to unforeseen side-effects.[16]

Derivates of Forskolin have been developed, FD-1 (6-{N-{2-isothiocyanatoethyl}aminocarbonyl}forskolin) has affinity for type II receptors and also III, V to lesser degrees. 5,6-dehydroxy-7-deacetyl-7-nicotinoylforskolin (FD-4) appears to have high affinity for type III receptors and no difference between II and V. Finally, 6-{3-(Dimethylamino)propionyl}14,15-dihydroforskolin appears to have great affinity for type V over type II, with lesser effects on type III.[16] This information is relevant as type II are ubiquitous (everywhere), type III are more located to olfactory tissues, atria and brown fat, and type V is the major isoform of the adult cardiac tissue.[17][16] Potencies of some of these isoforms relative to parent forskolin range from 100-300%.[16]


Molecular Targets


Adenylyl Cyclase

Forskolin is an adenylyl cyclase (synonymous with adenylate cyclase) stimulator, which increases levels of cyclic adenosine monophosphate (cAMP) in cells.[18][14] It is a highly reliable and effective cAMP increasing agent, and is routinely used as a research tool to investigate the effects of cAMP increases in a cell.[8]

This increase in cAMP does not increase lipolysis per se at low concentrations of 0.1-1µM, but when it surpasses 10µM it can induce lipolysis on its own.[18] Low concentrations are effective at increasing lipolysis when paired with β2-adrenergic agonists, suggesting the fat burning effects of forskolin are dependent on either high dosages or costimulation with other agents (exogenous and/or endogenous).[18] Similar to the costimulatory effect with agents that would normally stimulate adenylyl cyclase, pharmacological targets that can inherently suppress adenylyl cyclase activity such as α2-adrenergic stimulation or insulin can suppress the activity of forskolin in increasing cAMP.[19]

Forskolin can activate adenylyl cyclase to increase cAMP concentrations in a cell, and is additive with other agents that eventually increase cAMP. Endogenous molecules or supplements that exert a suppressive action on cAMP (via suppression of adenylyl cyclase) can suppress the activity of forskolin


Increasing cAMP

This mechanism of increasing cAMP is similar to exercise in regards to increasing activity of some enzymes, downstream of mitochondrial biogenesis (also, a non-significant increase in mitochondrial density at 4uM forskolin).[20] This cAMP increasing ability by Forskolin also appeared to non-significantly activate AMPK.[20]





Coleus Forskohlii is well absorbed in the cat gastrointestinal tract after oral administration[21] and can be absorbed in all areas of the intestines and colon (in rats) although the duodenum seems to have highest uptake.[22]

Forskolin appears to be subject to P-Glycoprotein efflux in the intestines, and coingestion of a P-glycoprotein inhibitor may increase oral bioavailability.[22]




Adenosinergic Neurotransmission

One study has found that adenosine signalling was required for forskolin (1µM) to increase cAMP in cerebral cortex slices of the rat, as the addition of caffeine was able to inhibit forskolin with an IC50 of 21+/-3µM.[23][24] This is likely due to the signalling properties of adenosine receptors, as increasing adenosine[25][26] or other adenosine receptor agonists[26] outside the cell increases the potency of forskolin while theophylline (weaker adenosine receptor antagonist) has much weaker effects.[23] When tested in hippocampal cells it seems that while activation of A1 adenosine receptors suppresses AMP accumulation from forskolin that A2 receptors stimulate it;[26] replicated in cerebral cortex slices.[27][28]

Activation of adenosine (A2) receptors seem to increase the ability of forskolin to accumulate cAMP in some neuronal cells, while blocking these receptors (notably with caffeine) reduces the potency of forskolin


Cholinergic Neurotransmission

Coleus leaves appear to have acetylcholinesterase inhibiting properties with an IC50 value of 1.02+/-0.02mg/mL in vitro[12][3] which appears to survive simulated gastric digestion[12] and has been noted to be relevant following oral ingestion of 600mg/kg in rats.[11]

These effects are thought to be secondary to rosmarinic acid which has an IC50 value of 0.44mg/mL, and the inhibition appears to be reversible.[11][3] Rosmarinic acid has been detected in the brain (20.4-24.1μM 30-60 minutes after intraperitoneal injection of 1g/kg) following ingestion of coleus leaf tea and acetylcholinesterase activity has been noted to be decreased by 5.5-10% (60 minute and 30 minutes, respectively).[11] Acetylcholineasterase inhibition has also been noted with isolated rosmarinic acid to the level of 12.8-13.5% following ingestion of 550μmol/kg.[11]

Coleus forskohlii leaves (not commonly supplemented, as many supplements contain the root) appear to have acetylcholinesterase inhibiting properties due to the rosmarinic acid content. These effects are confirmed in vivo


Interactions with Obesity


Human studies

In regards to human in vivo studies, they appear to be promising but limited in numbers and power. One study in overweight women noted that two doses of 250mg 10% extract reduced weight gain.[29] There was not significant weight loss in the experimental group, but there was a significant difference between the experimental (slight loss) and control (weight gain).[29] In overweight men, the same dose appears to cause favorable changes in body composition over a period of 12 weeks.[30] Testosterone and bone mass were also increased in the Coleus Forskohlii group. One study that did not investigate weight changes primarily noted that over a period of 2 months with 500-700mg Coleus Forskohlii there was a 2.38-2.6% reduction in BMI.[31]

There may be notable differences between obese and normal weight humans, as obese persons seem to have lower activity adenylate cyclase enzymes in fat cells, which is partially corrected upon weight loss via caloric restriction.[32] Also, men may have more benefit than women as testosterone can act as a fat burner/muscle preserving agent, although only one study has been conducted on men so far.[30]


Metabolic Rate

One study on overweight men consuming 250mg of Coleus Forskohlii twice daily found no significant effect on increasing the metabolic rate.[30]


Interactions with Skeletal Muscle


Muscle Protein Synthesis

Forskolin is able to increase activity of Adenylate Cyclase in skeletal muscle.[33] Through increasing cAMP, it has been speculated that Forskolin can increase muscle protein synthesis by activating PI3K and Akt, independent of the insulin receptor[34] and that this reaction is subject to desensitization.[35]


Muscle contractility

Forskolin, in vitro at concentrations of 1uM, has been shown to increase electical-stimulated skeletal muscle contractility in the mouse diaphragm.[36][37] The theorized mechanims of this is increasing cAMP levels, inducing PKA activity which acts on the ryanodine receptor and increases Ca2+ efflux from the sarcoplasmic reticulum. [38]

Although biological plausibility exists, no studies have been conducted on Coleus Forskohlii and muscle contraction in vivo.


Nutrients and Muscle cells

Forskolin has been implicated in vivo in reducing insulin's effects on the mTOR/Akt pathway in skeletal muscle.[39] Specifically, Forskolin appeared to reduce insulin's ability to phosphorylate Akt (with no affect on total Akt) and similar results were seen when looking at 4EBP1, with mTOR and S6K1 unaffected by all treatments.[39]

Forskolin is also able to inhibit myocyte GLUT4 translocation in vitro, and GLUT1 to a lesser degree.[40] This may also be downstream of cAMP, as it is seen in adipocytes as cAMP is known to adversely influence GLUT4 translocation via its promoter,[41][42] and also in muscle cells.[43]

In regards to fat metabolism, the activation of cAMP/PKA in myocytes seems to improve lipid metabolism,[44] and is one of the junction points of exercise and health in muscle cells.[45][46][47] Possibly through a myokine called Myonectin.[48]


Interactions with Heart Health


Blood Pressure

The active compound of Coleus Forskohlii, Forskolin, appears to either relax blood vessels and depress blood pressure or to have no overall effect on blood pressure.

It does not appear to reduce blood pressure via cholinergic or histamine means,[21] and provides a sustained reduction in blood pressure at 0.1-1mg/kg bodyweight in anathesized cats; with more reduction seen in those with higher baseline blood pressures.[21] Higher dosages do not increase potency of the blood pressure decrease, but instead prolong the time it can act; a parallel to the effects of forskolin on intraocular pressure.[21]

This vasorelaxant ability of forskohlii may be synergystic with Prostaglandin E1.[49]


Cardiac tissue

Forskolin is able to activate Adenylate Cyclase in the myocardium, and exerts a positive ionotropic effect which may be beneficial to failing hearts.[50] This has been observed in vivo with cat and rabbit hearts.[21]


Peripheral Organ Systems



One study noted decreases in Intra-Ocular Pressure (IOP) with forskohlin in human subjects given eyedrops containing the compound (1% of a 50µL solution)[51] via its effects as an adenylate cyclate activator.[52][53] It has been suggested that the role of forskolin is in enhancing the responsiveness of retinal ganglion cells (RGCs) to the stimulation from BDNF, as BDNF signals via cAMP in these cells[54][55] but increasing extracellular levels of BDNF are acutely effective in regenerating these cells[56] but are met with downregulation of its receptor TrkB.[57][58]

BDNF signalling in retinal cells works as a growth factor and uses cAMP as an intermediate in its signalling pathway. As chronic exposure to BDNF and its mimetics may reduce the expression of its receptor it is thought that downstream stimulation (via forskolin) could have similar efficacy without the risk of tolerance

Oral studies using forskolin have been confounded with other compounds. A reduction in IOP has been noted with oral ingestion of coleus forskohlii (200mg of 10% forskolin) alongside 200mg rutin and two B-vitamins (thiamin and riboflavin at 550µg and 700µg respectively) by approximately 20% after 40 days in subjects with primary open angle glaucoma (POAG)[59] while other studies using this formulation have replicated its findings[60] and seems effective when given in addition to their standard (topical) therapy where the supplement over one month reduced IOP by an average of 10%.[61]

Studies lasting upwards of 40 days have found forskolin to be effective in reducing intraocular pressure when orally administered at supplemental doses. More studies are needed using forskolin alone (as the mentioned studies have confounds) and perhaps longer periods of time to properly assess the tolerance issue



Coleus Forskohlii extract at 0.5% of feed intake in rats results in induction of various enzyme systems in the liver, alongside an increase in liver weight. Dose dependent increases in transcription for Cyp2b10, Cyp2c29, Cyp3a11, and Gstm2 were noted.[62] These changes were seen after 1 week, and ceased upon cessation of Coleus intake. This intake was estimated to be 740mg/kg bodyweight of Coleus daily; 24mg in total for the rats.[62] The CYP2C induction is of clinical relevance, as it is the enzyme that metabolizes warfarin.

Isolated forskolin has weaker induction of CYP3A and Glutathione enzymes, and does not increase liver weight at 0.05% of the diet.[62] This induction may be mediated by agonism of the Pregnane X receptor, which is independent of its activities on Adenylate Cyclase.[63]


Interactions with Hormones



One intervention in overweight men noted increases in testosterone with 250mg Coleus Forskohlii (10% Forskolin by weight) over the course of 12 weeks.[30] Although there were significant differences at baseline (5.06+/-1.21ng versus 4.12+/-0.82ng Total Test, 15.90+/-13.39pg v. 13.28+/-7.26pg free test; higher values in Coleus group) increases were still at 6 weeks and 12 weeks in Coleus while no changes occurred in control. Total test increased by 16.77+/-33.77% and free test by 3.47+/-8.10 after 12 weeks, with high inter-individual variance.[30]

The hypothesized mechanism of action is via increasing intra-testicular cAMP levels, which mimick the mechanisms of action of luteinizing hormone in the testicles.[64] LH normally increases cAMP itself, but circumventing LH to increase cAMP can increased steroidogenesis per se.[65][66] Even some other studies investigating herbs like Cordyceps in the testes will use forskolin as a standard by which to compare the efficacy of the newer drugs.[67]

Coleus extract may also induce CYP3A4 in the liver, which theoretically should lead to increased metabolism of testosterone.[62] However, testosterone was not measured in this rat study; isolated forskolin had a much lesser effect.



Forskolin has been shown, in vitro, to be able to release insulin (as well as glucagon and somatostatin) when incubated in pancreatic cells.[68]


Nutrient-Nutrient Interactions


Beta-Adrenergic Agonists

Its is able to potentiate the effects of the beta-adrenergic agonist isoproterenol, and seems to be highly effective until isoproterenol reaches concentrations of 1uM (in which afterwards, descending returns are seen),[18] forskolin showed dose dependent benefits in increasing cAMP alongside isoproterenol.

In situations where beta-adrenergic agonists do not stimulate (hyporesponsiveness), low doses of forskolin are able to rescue the effectiveness of beta-adrenergic agonists.[69] Additionally, 1uM forskolin (although not lesser concentrations) are able to rescue beta-adrenergic desensitization.[70]

This synergy has been noted in vivo using isoproterenol and forskolin, via IV.[71]

Beta-Adrenergic agonists incluce synephrine, ephedrine, capsaicin and possibly raspberry ketones; as well as endogenous adrenaline secretion.



Forskolin is synergistic with methylxanthines, as methylxanthines have the ability to reduce adenosine's suppressive influence on elevated cAMP levels in adipocytes via acting as adenosine inhibitors.[72][18] This combination of Forskolin and the Methylxanthine Aminophylline is even more synergistic with the addition of a beta-adrenergic agonist, such as ephedrine.

Some methylxanthines, such as theophylline and caffeine, also possess phosphodiesterase inhibitory properties. PDE inhibition results in increased cAMP by alleviating degradation, and forskolin does not influence PDEs.[18] The combination of methylxanthines and forskolin can increase production of and alleviate degradation of cAMP to promote synergism in vitro.

Forskolin has also been shown to increase sarcoplasmic loading of Calcium and modulate Calcium spikes from the sarcoplasmic reticulum (via phospholambin)[73] which augments caffeine's ability to induce calcium release.[74]

Methylxanthines include theophylline, theobromine, and caffeine. These can be found in high amounts in tea, chocolate, and coffee; respectively.


Alpha-Adrenergic Antagonists

When coincubated (in the cell at the same time), and alpha-adrenergic agonism by insulin or agonists can inhibit the increases in cAMP seen by forskolin.[75] Co-incubation of an alpha-adrenergic antagonist with the agonist and forskolin can rescue some of the effects by negating the inhibition.[75]

Interestingly, sensitizing cells (in this study, colonic carcinoma cells) by incubating with an alpha-adrenergic agonist [75] After exposure to an agonist for 30+ minutes, cells have 20-fold increases in forskolin-stimulated cAMP for a short time (20-40 minutes).[75][76]


Safety and Toxicity



Coleus Forskohlii supplementation can cause an increase in stomach acid levels, and may be a bad idea for those currently suffering from stomach ulcers.[77]

In cats, the LD50 appears to be 68mg/kg bodyweight forskolin.[21]



Aortic cells normally increase calcium uptake in response to cAMP, although it appears that a 20 hour incubation of 25µM forskolin can desensitize these cells to stimulation from cAMP despite adenylyl cyclase not being desensitized, suggesting refractory adaptation on another level.[78] Other cells have noted refractoriness at the level of protein synthesis and can be mimicked by isoproterenol (β2-adrenergic agonist).[79]

It seems that while adenylyl cyclase itself is not desensitized or altered in function with exposure to forskolin, prolonged elevations of cAMP cause proteins to be synthesized in an attempt to normalize intracellular cAMP levels.

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