Hypericum perforatum

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Hypericum perforatum
Saint John's wort flowers.jpg
Scientific classification e
Kingdom: Plantae
Clade: Angiosperms
Clade: Eudicots
Clade: Rosids
Order: Malpighiales
Family: Hypericaceae
Genus: Hypericum
Species: H. perforatum
Binomial name
Hypericum perforatum

Hypericum perforatum, known as perforate St John's-wort,[1] common Saint John's wort and St John's wort,[note 1] is a flowering plant in the family Hypericaceae. The common name "St John's wort" may be used to refer to any species of the genus Hypericum. Therefore, Hypericum perforatum is sometimes called "common St John's wort" or "perforate St John's wort" to differentiate it. It is a believed to be a medicinal herb with antidepressant activity, although high-quality clinical evidence for such effects is limited.

The primary pharmacologically active constituent of St John's wort, hyperforin, is an arachidonate 5-lipoxygenase inhibitor and COX-1 inhibitor in vitro.[3][4][5]

Botanical description[edit]

Translucent dots of glandular tissue on the leaves

Hypericum perforatum is native to parts of Europe and Asia[6] but has spread to temperate regions worldwide as a cosmopolitan invasive weed.

The common name "St John's wort" comes from its traditional flowering and harvesting on St John's Day, 24 June. The genus name Hypericum is derived from the Greek words hyper (above) and eikon (picture), in reference to the tradition of hanging plants over religious icons in the home during St John's Day, to ward off evil.

Perforate St John's wort is a herbaceous perennial plant with extensive, creeping rhizomes. Its stems are erect, branched in the upper section, and can grow to 1 m high. It has opposite, stalkless, narrow, oblong leaves that are 1–2 cm long.[7]:176 The leaves are yellow-green in color, with scattered translucent dots of glandular tissue.[8] The dots are conspicuous when held up to the light, giving the leaves the 'perforated' appearance to which the plant's Latin name refers. The flowers measure up to 2.5 cm across, have five petals, and are colored bright yellow with conspicuous black dots.[9]:339 The flowers appear in broad cymes at the ends of the upper branches, between late spring and early to mid summer. The sepals are pointed, with black glandular dots. There are many stamens, which are united at the base into three bundles. The pollen grains are ellipsoidal.[2]

When flower buds (not the flowers themselves) or seed pods are crushed, a reddish/purple liquid is produced.[10]


St John's wort reproduces both vegetatively and sexually. It thrives in areas with either a winter- or summer-dominant rainfall pattern; however, distribution is restricted by temperatures too low for seed germination or seedling survival. Altitudes greater than 1500 m, rainfall less than 500 mm, and a daily mean temperature greater than 24 °C are considered limiting thresholds.[who?] Depending on environmental and climatic conditions, and rosette age, St John's wort will alter growth form and habit to promote survival. Summer rains are particularly effective in allowing the plant to grow vegetatively, following defoliation by insects or grazing.

The seeds can persist for decades in the soil seed bank, germinating following disturbance.[11]

Invasive species[edit]

Although Hypericum perforatum is grown commercially in some regions of south east Europe, it is listed as a noxious weed in more than twenty countries and has introduced populations in South and North America, India, New Zealand, Australia, and South Africa.[11] In pastures, St John's wort acts as both a toxic and invasive weed. It replaces native plant communities and forage vegetation to the extent of making productive land nonviable[12] or becoming an invasive species in natural habitats and ecosystems. Ingestion by livestock such as horses, sheep, and cattle can cause photosensitization, central nervous system depression, spontaneous abortion or death.[12][13] Effective herbicides for control of Hypericum include 2,4-D, picloram, and glyphosate. In western North America three beetles Chrysolina quadrigemina, Chrysolina hyperici and Agrilus hyperici have been introduced as biocontrol agents.[14]

Traditional medicine[edit]

Common St. John's wort has long been used in herbalism and folk medicine.[15] It was thought to have medical properties in classical antiquity and was a standard component of theriacs, from the Mithridate of Aulus Cornelius Celsus' De Medicina (ca. 30 CE) to the Venice treacle of d'Amsterdammer Apotheek in 1686. Folk usages included oily extract ("St. John's oil") and Hypericum snaps.Hypericum perforatum is a common species and is grown commercially for use in herbalism and traditional medicine.[16]

The red, oily extract of H. perforatum may help heal wounds.[15][17] Both hypericin and hyperforin are under study for their potential antibiotic properties.[18]

Modern phytotherapy[edit]

Some studies have supported the efficacy of St John's wort as a treatment for depression in humans, but have not concluded it as a replacement for more studied treatments, and proper medical consultation.[15][19] A 2015 meta-analysis review concluded that it has superior efficacy to placebo in treating depression, is as effective as standard antidepressant pharmaceuticals for treating depression, and has fewer adverse effects than other antidepressants.[20] The authors concluded that it is difficult to assign a place for St. John's wort in the treatment of depression owing to limitations in the available evidence base, including large variations in efficacy seen in trials performed in German-speaking relative to other countries. In Germany, St. John's wort may be prescribed for mild to moderate depression, especially in children and adolescents.[21] A 2008 Cochrane review of 29 clinical trials concluded that it was superior to placebo in patients with major depression, as effective as standard antidepressants and had fewer side-effects.[22]

According to the United States National Center for Complementary and Integrative Health, "St. John’s wort isn’t consistently effective for depression."[15] A 2016 review noted that use of St. John's wort for mild and moderate depression was better than placebo for improving depression symptoms, but not better than using antidepressant medication.[23]

Side effects[edit]

St. John’s wort can interact in dangerous, sometimes life-threatening ways with a variety of prescribed medicines.[15] St John's wort is generally well tolerated, but may cause gastrointestinal discomfort, such as (nausea, abdominal pain, loss of appetite, and diarrhea), dizziness, confusion, fatigue, sedation, dry mouth, restlessness, and headache.[24][25][26][27]

The organ systems associated with adverse drug reactions to St John's wort and fluoxetine (an SSRI) have a similar incidence profile;[28] most of these reactions involve the central nervous system.[28] St John's wort also decreases the levels of estrogens, such as estradiol, by accelerating its metabolism, and should not be taken by women on contraceptive pills.[15] St John's wort may cause photosensitivity. This can lead to visual sensitivity to light and to sunburns in situations that would not normally cause them.[24]


St. John’s wort can interfere with the effects of many prescription medicines, including birth control pills, cyclosporine, digoxin, HIV drugs, cancer medications including irinotecan, and warfarin.[15] Combining both St John's wort and antidepressants could lead to increased serotonin levels causing serotonin syndrome.[29] It should not be taken with the heart medication, ranolazine.[30] Combining estrogen containing oral contraceptives with St John's wort can lead to decreased efficacy of the contraceptive and eventually unplanned pregnancies.[31] Consumption of St. John's wort is discouraged for those with bipolar disorder. There is concern that people with bipolar depression taking St. John's wort may be at a higher risk for mania.[32]


St John's wort has been shown to cause multiple drug interactions through induction of the cytochrome P450 enzymes CYP3A4 and CYP1A2. This drug-metabolizing enzyme induction results in the increased metabolism of certain drugs, leading to decreased plasma concentration and potential clinical effect.[33] The principal constituents thought to be responsible are hyperforin and amentoflavone. There is strong evidence that the mechanism of action of these interactions is activation of the pregnane X receptor.[34]

St John's wort has also been shown to cause drug interactions through the induction of the P-glycoprotein efflux transporter. Increased P-glycoprotein expression results in decreased absorption and increased clearance of certain drugs, leading to lower plasma concentrations and impaired clinical efficacy.[35]

Examples of drugs whose effectiveness may be reduced by St. John's wort
Class Drugs
Antiretrovirals Non-nucleoside reverse transcriptase inhibitors, protease inhibitors
Benzodiazepines Alprazolam, midazolam
Hormonal contraception Combined oral contraceptives
Immunosuppressants Calcineurin inhibitors, cyclosporine, tacrolimus
Antiarrhythmics Amiodarone, flecainide, mexiletine
Beta-blockers Metoprolol, carvedilol
Calcium channel blockers Verapamil, diltiazem, amlodipine, pregabalin
Statins (cholesterol-reducing medications) Lovastatin, simvastatin, atorvastatin
Others Digoxin, methadone, omeprazole, phenobarbital, theophylline, warfarin, levodopa, buprenorphine, irinotecan
Reference: Rossi, 2005; Micromedex

For a complete list, see CYP3A4 ligands and CYP2C9 ligands.

In vitro research and phytochemicals[edit]

St. John's wort, similarly to other herbs, contains different chemical constituents.[36] Hyperforin and adhyperforin, two phloroglucinol constituents of St John's wort, are TRPC6 receptor agonists and, consequently in laboratory experiments, they induce noncompetitive reuptake inhibition of monoamines (specifically, dopamine, norepinephrine, and serotonin), GABA, and glutamate when they activate this ion channel.[19][37][38] Hyperforin is also under basic research for its possible anti-inflammatory properties.[37][38][39] Moreover, St John's wort downregulates the β1 adrenoceptor and upregulate postsynaptic 5-HT1A and 5-HT2A receptors in vitro.[19]

Comparison of selected active chemical constituents of Hypericum perforatum[36][40]
Compound Conc.[36]
log P PSA pKa Formula MW CYP1A2
[Note 1]
[Note 2]
[Note 3]
[Note 4]
[Note 5]
t1/2[42] (h) Tmax[42] (h) Cmax[42] (mM) CSS[42] (mM) Notes/Biological activity[Note 6]
Phloroglucinols (2-5%)
Adhyperforin 0.2-1.9 10-13 71.4 8.51 C36H54O4 550.81 ? ? ? ? ? ? ? ? ? Inhibits reuptake of: 5-HT, DA, NE, GABA and Glu via TRPC6 activation[43]
Hyperforin 2-4.5 9.7-13 71.4 8.51 C35H52O4 536.78 +[44] +[44]/-[45] -[45] + + 3.5-16 2.5-4.4 15-235 53.7 Serves as a TRPC6 and PXR agonist. Reuptake inhibitor of 5-HT (205nM), DA (102nM), NE (80nM), GABA (184nM), Glu (829nM), Gly and Ch (8.5μM). Angiogenesis, COX-1 (300nM), 5-LO (90nM), SIRT1 (15μM), SIRT2 (28μM) and MRSA (1.86μM) inhibitor.
Naphthodianthrones (0.03-3%)
Hypericin[46] 0.003-3 7.5-10 156 6.9±0.2 C30H16O8 504.44 0 -
(3.4 μM)
- (8.5 μM) -
(8.7 μM)
? 2.5-6.5 6-48 0.66-46 ? Is a topoisomerase II,[47] PKA (10μM), PKC (27nM), CK1 (3μM), CK2 (6nM), MAPK (4nM), EGFR (35nM), InsR (29nM), PI3K (180nM), DBH (12.4μM), DNA polymerase A (14.7μM), HIV-1 RT (770nM), COMT, MAOA (68μM) and MAOB (420μM), succinoxidase (8.2μM), GSR (2.1nM), GPx (5.2μM), GST (6.6μM) and CuZnSOD (5.25μM) inhibitor.[42][46] Binds to the NMDA receptor (Ki=1.1μM), μ-opioid, κ-opioid, δ-opioid, 5-HT6, CRF1, NPY-Y1, NPY-Y2 and σ receptors.[46] Exhibits light-dependent inhibitory effects on HIV-1 and cancers.[46]
Pseudohypericin 0.2-0.23 6.7±1.8 176 7.16 C30H16O9 520.44 ? ? ? ? ? 24.8-25.4 3 1.4-16 0.6-10.8[48] Photosensitiser and antiretroviral like hypericin.[49][50] PKC inhibitory effects in vitro.[51]
Flavonoids (2-12%)
0.01-0.05 3.1-5.1 174 2.39 C30H18O10 538.46 ? -
(35 nM)
- (24.3 μM) -
(4.8 μM)
? ? ? ? ? Serves as a fatty acid synthase (FASN) inhibitor,[53][54][55] kappa opioid antagonist,[56] and a negative allosteric modulator at the benzodiazepine site of the GABAA receptor.[57]
Apigenin 0.1-0.5 2.1±0.56 87 6.63 C15H10O5 270.24 ? ? ? ? ? ? ? ? ? Benzodiazepine receptor ligand (Ki=4μM) with anxiolytic effects.[58] Also has anti-inflammatory, anticancer, cancer-preventing and antioxidant effects.[59][60]
Catechin 2-4 1.8±0.85 110 8.92 C15H14O6 290.27 ? ? ? ? ? ? ? ? ? Anticancer, antioxidant, cardioprotective and antimicrobial.[61][62] Cannabinoid receptor CB1 ligand.[63]
Epigallocatechin ? -0.5-1.5 131 8.67 C15H14O6 290.27 ? ? ? ? ? 1.7±0.4a 1.3-1.6a ? ? Found in higher concentrations in Green tea. Antioxidant. CB1 receptor ligand (Ki=35.7 μM).[63]
Hyperoside 0.5-2 1.5±1.7 174 6.17 C21H20O12 464.38 ? ? -[64] (3.87μM) ? ? ? ? ? ? Has anti-fungal effects in vitro (against the plant pathogens P. guepini and Drechslera),[65] neuroprotective effects via the PI3K/Akt/Bad/BclXL signalling pathway in vitro,[66] anti-inflammatory effects via NF-κB inhibition in vitro,[67] D2 receptor-dependent antidepressant-like effects in vivo,[68] and antiglucocorticoid-like effects in vitro.[69]
Kaempferol[70] ? 2.1±0.6 107 6.44 C15H10O6 286.24 ? ? ? +/-[Note 7] ? ? ? ? ? Inhibits the following: inflammation (via NF-κB and STAT1 inhibition),[71] cancer, HDAC,[72] bacteria, viruses, protozoa and fungi.[73] It is also known to prevent cardiovascular disease and cancer.[73]
Luteolin ? 2.4±0.65 107 6.3 C15H10O6 286.24 - ? ? ? ? ? ? ? ? Has anti-inflammatory, anticancer, anti-allergic and antioxidant effects.[74][75] May also have positive effects on people with autism spectrum disorders.[76] Potent non-selective competitive inhibitor of PDE1-5.[77]
Quercetin[78][79] 2-4 2.2±1.5 127 6.44 C15H10O7 302.24 -
(7.5 μM)
- (47 μM)
- (24 μM)
- (22 μM)
- 20-72c 8c ? ? Has anti-cancer, anti-inflammatory, anti-allergic, anti-asthmatic, antihypertensive, analgesic, neuroprotective, gastroprotective, anti-diabetic, cardiovascular disease-preventing, antioxidant, antidepressant-like (in rat models of depression), anxiolytic-like, sedative, antimicrobial and athletic performance-promoting effects.[79] Non-selective PDE1-4 inhibitor that is slightly selective for PDE3/4 over PDE1/2.[80]
Rutin 0.3-1.6 1.2±2.1 266 6.43 C27H30O16 610.52 ? ? ? ? ? ? ? ? ? Has anticancer, cardioprotective, nephroprotective, antioxidant, anti-inflammatory, antidiabetic, procognitive and antilipidaemic effects.[81]
Phenolic acids (~0.1%)
Caffeic acid 0.1 1.4±0.4 77.8 3.64 C9H8O4 180.16 ? ? ? -[82] ? ? ? ? ? Anticancer, hepatoprotective, antibacterial and antioxidant effects reported.[83]
Chlorogenic acid <0.1% -0.36±0.43 165 3.33 C16H18O9 354.31 0 0 0 0 ? ? ? ? ? Antibacterial, anticancer and antioxidant effects have been demonstrated.[84]
Acronyms and symbols
Acronym/Symbol Meaning
MW Molecular weight in g•mol−1.
PGP P-glycoprotein
t1/2 Elimination half-life in hours
Tmax Time to peak plasma concentration in hours
Cmax Peak plasma concentration in mM
CSS Steady state plasma concentration in mM
Partition coefficient.
PSA Polar surface area of the molecule in question in square angstroms2). Obtained from PubChem (the access date is 13 December 2013).
Conc. These values pertain to the approximation concentration (in %) of the constituents in the fresh plant material
- Indicates inhibition of the enzyme in question.
+ Indicates an inductive effect on the enzyme in question.
0 No effect on the enzyme in question.
5-HT 5-hydroxytryptamine — synonym for serotonin.
DA Dopamine
NE Norepinephrine
GABA γ-aminobutyric acid
Glu Glutamate
Gly Glycine
Ch Choline
a Pharmacokinetic data for ECG comes from a study[85] of its pharmacokinetics after oral administration of green tea.
b Comes from this source.[45]
c Pharmacokinetic data for quercetin comes from a study[86] using pure oral quercetin, not a St John's wort extract.


  1. ^ In brackets is the IC50/EC50 value depending on whether it is an inhibitory or inductive action being exhibited, respectively.
  2. ^ As with last note
  3. ^ As with last note
  4. ^ As with last note
  5. ^ As with last note
  6. ^ Values given in brackets are IC50/EC50 depending on whether it's an inhibitory or inductive action the compound displays towards the biologic target in question. If it pertains to bacterial growth inhibition the value is MIC50
  7. ^ Depends on the time frame: short-term administration causes inhibition; long-term causes induction via PXR



In large doses, St John's wort is poisonous to grazing livestock (cattle, sheep, goats, horses).[12] Behavioural signs of poisoning are general restlessness and skin irritation. Restlessness is often indicated by pawing of the ground, headshaking, head rubbing, and occasional hindlimb weakness with knuckling over, panting, confusion, and depression. Mania and hyperactivity may also result, including running in circles until exhausted. Observations of thick wort infestations by Australian graziers include the appearance of circular patches giving hillsides a 'crop circle' appearance, it is presumed, from this phenomenon. Animals typically seek shade and have reduced appetite. Hypersensitivity to water has been noted, and convulsions may occur following a knock to the head. Although general aversion to water is noted, some may seek water for relief.

Severe skin irritation is physically apparent, with reddening of non-pigmented and unprotected areas. This subsequently leads to itch and rubbing, followed by further inflammation, exudation, and scab formation. Lesions and inflammation that occur are said to resemble the conditions seen in foot and mouth disease. Sheep have been observed to have face swelling, dermatitis, and wool falling off due to rubbing. Lactating animals may cease or have reduced milk production; pregnant animals may abort. Lesions on udders are often apparent. Horses may show signs of anorexia, depression (with a comatose state), dilated pupils, and injected conjunctiva.


Increased respiration and heart rate is typically observed while one of the early signs of St John's wort poisoning is an abnormal increase in body temperature. Affected animals will lose weight, or fail to gain weight; young animals are more affected than old animals. In severe cases death may occur, as a direct result of starvation, or because of secondary disease or septicaemia of lesions. Some affected animals may accidentally drown. Poor performance of suckling lambs (pigmented and non-pigmented) has been noted, suggesting a reduction in the milk production, or the transmission of a toxin in the milk.


Most clinical signs in animals are caused by photosensitisation.[87] Plants may induce either primary or secondary photosensitisation:

  • primary photosensitisation directly from chemicals contained in ingested plants
  • secondary photosensitisation from plant-associated damage to the liver.

Araya and Ford (1981) explored changes in liver function and concluded there was no evidence of Hypericum-related effect on the excretory capacity of the liver, or any interference was minimal and temporary. However, evidence of liver damage in blood plasma has been found at high and long rates of dosage.

Photosensitisation causes skin inflammation by a mechanism involving a pigment or photodynamic compound, which when activated by a certain wavelength of light leads to oxidation reactions in vivo. This leads to lesions of tissue, particularly noticeable on and around parts of skin exposed to light. Lightly covered or poorly pigmented areas are most conspicuous. Removal of affected animals from sunlight results in reduced symptoms of poisoning.


Detection in body fluids[edit]

Hypericin, pseudohypericin, and hyperforin may be quantitated in plasma as confirmation of usage and to estimate the dosage. These three active substituents have plasma elimination half-lives within a range of 15–60 hours in humans. None of the three has been detected in urine specimens.[88]

Chemical constituents[edit]

Chemical structure of hypericin

The plant contains the following:[36][41]

The naphthodianthrones hypericin and pseudohypericin along with the phloroglucinol derivative hyperforin are thought to be among the numerous active constituents.[2][89][90][91] It also contains essential oils composed mainly of sesquiterpenes.[2]


A major constituent chemical, hyperforin, may be useful for treatment of alcoholism, although dosage, safety and efficacy have not been studied.[92][93] Hyperforin has also displayed antibacterial properties against Gram-positive bacteria, although dosage, safety and efficacy has not been studied.[94] Herbal medicine has also employed lipophilic extracts from St John's wort as a topical remedy for wounds, abrasions, burns, and muscle pain.[93] The positive effects that have been observed are generally attributed to hyperforin due to its possible antibacterial and anti-inflammatory effects.[93] For this reason hyperforin may be useful in the treatment of infected wounds and inflammatory skin diseases.[93] In response to hyperforin's incorporation into a new bath oil, a study to assess potential skin irritation was conducted which found good skin tolerance of St John's wort.[93]

See also[edit]


  1. ^ Less common names and synonyms include Tipton's weed, rosin rose, goatweed, chase-devil, or Klamath weed.[2]


  1. ^ "BSBI List 2007". Botanical Society of Britain and Ireland. Archived from the original (xls) on 25 January 2015. Retrieved 17 October 2014. 
  2. ^ a b c d Mehta, Sweety (2012-12-18). "Pharmacognosy of St. John's Wort". Pharmaxchange.info. Retrieved 2014-02-16. 
  3. ^ "Enzymes". Hyperforin. Human Metabolome Database. 3.6. University of Alberta. 30 June 2013. Retrieved 12 December 2014. Hyperforin is found in alcoholic beverages. Hyperforin is a constituent of Hypericum perforatum (St John's Wort) Hyperforin is a phytochemical produced by some of the members of the plant genus Hypericum, notably Hypericum perforatum (St John's wort). The structure of hyperforin was elucidated by a research group from the Shemyakin Institute of Bio-organic Chemistry (USSR Academy of Sciences in Moscow) and published in 1975. Hyperforin is a prenylated phloroglucinol derivative. Total synthesis of hyperforin has not yet been accomplished, despite attempts by several research groups. Hyperforin has been shown to exhibit anti-inflammatory, anti-tumor, antibiotic and anti-depressant functions (PMID 17696442, 21751836, 12725578, 12018529)
    1. Arachidonate 5-lipoxygenase ...Specific function: Catalyzes the first step in leukotriene biosynthesis, and thereby plays a role in inflammatory processes ...
    2. Prostaglandin G/H synthase 1 ... General function: Involved in peroxidase activity
  4. ^ Wölfle U, Seelinger G, Schempp CM (2014). "Topical application of St. John's wort (Hypericum perforatum)". Planta Med. 80 (2–3): 109–20. doi:10.1055/s-0033-1351019. PMID 24214835. Anti-inflammatory mechanisms of hyperforin have been described as inhibition of cyclooxygenase-1 (but not COX-2) and 5-lipoxygenase at low concentrations of 0.3 µmol/L and 1.2 µmol/L, respectively [52], and of PGE2 production in vitro [53] and in vivo with superior efficiency (ED50 = 1 mg/kg) compared to indomethacin (5 mg/kg) [54]. Hyperforin turned out to be a novel type of 5-lipoxygenase inhibitor with high effectivity in vivo [55] and suppressed oxidative bursts in polymorphonuclear cells at 1.8 µmol/L in vitro [56]. Inhibition of IFN-γ production, strong downregulation of CXCR3 expression on activated T cells, and downregulation of matrix metalloproteinase 9 expression caused Cabrelle et al. [57] to test the effectivity of hyperforin in a rat model of experimental allergic encephalomyelitis (EAE). Hyperforin attenuated the symptoms significantly, and the authors discussed hyperforin as a putative therapeutic molecule for the treatment of autoimmune inflammatory diseases sustained by Th1 cells. 
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  16. ^ USDA.gov Retrieved November 23, 2015
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  18. ^ Schempp, Christoph M; Pelz, Klaus; Wittmer, Annette; Schöpf, Erwin; Simon, Jan C (1999). "Antibacterial activity of hyperforin from St John's wort, against multiresistant Staphylococcus aureus and gram-positive bacteria". The Lancet. 353 (9170): 2129. doi:10.1016/S0140-6736(99)00214-7. PMID 10382704. 
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