Is passionflower a scheduled substance in Australia?

Passiflora incarnata aerial parts are not scheduled under Australia's Poisons Standard, meaning they can be sold in listed complementary medicines (AUST L) on the ARTG without a prescription. However, isolated β-carboline alkaloids from the plant — such as harmine and harmaline — do appear in Schedule 9 at certain concentrations and in isolated form, so the whole-plant versus isolated-constituent distinction matters legally.

What are the main chemical constituents researchers have focused on?

The most studied constituents in Passiflora incarnata are the C-glycosyl flavonoids — particularly vitexin, isovitexin, orientin and chrysin — and the harmane β-carboline alkaloids (harman, harmine, harmaline). Chrysin has been examined for GABA-A receptor binding affinity in laboratory models, while the β-carbolines are known MAO inhibitors at sufficient concentration. The relative contribution of each fraction to any observed effects in human studies has not been definitively established.

What does an AUST L listing mean for a passionflower product?

An AUST L listing on the Australian Register of Therapeutic Goods (ARTG) means the TGA has accepted the ingredients as generally low-risk for the listed use, but has not evaluated that specific product for clinical efficacy. Listed passionflower products may carry only the TGA's permitted low-level indications — such as 'traditionally used as a mild nervine tonic' — and may not make claims about treating, preventing or curing any named medical condition.

Are there any known interaction concerns with passionflower?

The β-carboline alkaloids present in Passiflora incarnata have monoamine oxidase inhibitory (MAOI) properties at sufficient concentration, which is a potential pharmacological interaction point with prescription MAOIs and serotonergic medicines. Anyone taking pharmaceutical medicines should consult a registered pharmacist or medical practitioner before using passionflower preparations. This article does not constitute medical advice.

How does passionflower research compare to other nervine botanicals like kava?

The human clinical trial database for Passiflora incarnata is small — most trials involve fewer than 50 participants and short follow-up periods. Kava (Piper methysticum) has a larger, though still debated, clinical dataset, but carries a different regulatory status in Australia, including import permit requirements for personal use and specific hepatotoxicity warnings. Both plants sit in a category where ethnobotanical history is strong but high-quality clinical evidence remains limited.

Passionflower: Traditional Use, Constituents and Evidence

By Naomi Ellison · 29 June 2026 · 7 min read

2 men in white and blue uniform holding blue and white plastic toy

My nan had a passionflower vine crawling up the back fence in Stirling, and she'd harvest the dried aerial parts every summer with the kind of quiet certainty that made me assume it was simply a kitchen ingredient. It wasn't until I was older , reading through a battered 1880s edition of Potter's Cyclopaedia of Botanical Drugs and Preparations , that I started to understand what she was actually reaching for. The plant has a layered, genuinely interesting history, and the science behind it is more complicated than most supplement labels will tell you.

What is passionflower?

Passiflora incarnata L. is the species most extensively documented in phytomedicine research, though the genus Passiflora contains over 500 species, many of them used ethnobotanically across the Americas. The plant is native to the south-eastern United States and parts of Central and South America. The name , bestowed by Spanish missionaries in the 16th century; came from a fanciful reading of the flower's anatomy as symbolic of the Passion of Christ. The three stigmas as nails, the five stamens as wounds, the corona filaments as the crown of thorns. That story stuck.

The aerial parts (leaves, stems, sometimes flowers) are the portions used in herbal preparation. They can be dried and infused, extracted into hydroalcoholic tinctures, or concentrated into standardised extracts. Within the broad framework of phytomedicine, P. incarnata sits alongside other botanical anxiolytics that have attracted scientific scrutiny, kava (Piper methysticum), valerian and lemon balm, though each has a distinct chemical profile and a very different regulatory history in Australia.

Traditional and historical use

Indigenous peoples of what is now the south-eastern United States used P. incarnata long before European contact; the Cherokee documented uses of the root and leaf, and the plant was noted in early colonial-era pharmacopoeias. It entered formal European herbal practice in the 17th century after returning travellers brought specimens back, and by the late 19th century it appeared in the United States Pharmacopoeia (listed from 1898 to 1936).

In Australian traditional herbalism, passionflower arrived via British and European immigrant practice. It doesn't feature in First Nations botanical medicine here, that's an important distinction worth making clearly. Its local history is entirely a transplanted one.

European herbal tradition primarily employed it as a nervine: a plant used to quieten nervous excitability. The 19th-century literature is full of language that would never pass a modern regulatory filter, so I won't reproduce claims here. What's relevant is that this long period of documented use informed the research questions that came later.

Key constituents: flavonoids, alkaloids and beyond

Passiflora incarnata is chemically complex. The constituent classes most studied by researchers are:

Flavonoids, particularly chrysin, vitexin, isovitexin, orientin and isoorientin. Chrysin is the compound that has drawn the most pharmacological attention; it has been studied in cell and animal models for its affinity with GABA-A receptor binding sites, though translating that to human physiology is not straightforward.
Harmane alkaloids (β-carbolines); harman, harmine and harmaline are present in small amounts. These are monoamine oxidase inhibitors (MAOIs) in sufficient concentration and are the same alkaloid class found in the South American botanical preparation ayahuasca. The concentrations in P. incarnata aerial-part extracts are generally low, but this is worth knowing if someone is considering passionflower alongside prescription MAOIs or other serotonergic medicines, that's a conversation for a pharmacist or doctor.
Maltol and ethyl maltol, organic compounds contributing to flavour; some early studies proposed they contributed to sedative-adjacent activity but more recent analysis suggests they are not the primary active fraction.
Polysaccharides and organic acids; present, but less studied in the context of pharmacological activity.

The question of which constituent (or combination of constituents) drives the effects observed in clinical research is genuinely unsettled. This matters because standardised extracts have to standardise to something, and different manufacturers have historically standardised to different markers (total flavonoids, vitexin, or isovitexin), making cross-study comparison difficult. Honestly, the lack of agreed standardisation is one of the more frustrating gaps in the field.

It's also worth noting that passionflower's terpene fraction has received almost no systematic study. For context, terpenes in other botanical species, the kind documented in cannabis research and covered in our terpene glossary; are increasingly understood to modulate activity in ways that isolated constituents alone don't predict. Whether something analogous applies to P. incarnata's minor volatile fraction remains, as far as I can find, an open question.

What the clinical research actually shows (and its limits)

There have been a modest number of human clinical trials on P. incarnata, most small, most focused on anxiety-related endpoints. A 2001 randomised controlled trial published in the Journal of Clinical Pharmacy and Therapeutics compared a passionflower extract to oxazepam (a benzodiazepine) over four weeks in 36 participants. The extract performed comparably on anxiety rating scales, with fewer impairment-related side effects reported in the passionflower arm. But 36 participants over four weeks is a small study. You cannot draw firm conclusions from it, you can note it as an interesting signal that warrants larger investigation.

Other trials have examined passionflower in combination products (often with valerian and/or hops), which makes it harder to attribute any effect to a single constituent or even a single plant. A 2011 meta-analysis covering several nervine botanicals noted consistent methodological limitations: small sample sizes, short durations, varied extract preparations, and inconsistent outcome measures. The authors called for standardised extraction protocols before further large trials. A reasonable call.

Animal and in vitro studies have explored mechanisms involving GABA-A receptor binding (relevant to the chrysin data), and some have looked at interactions with bioavailability and first-pass metabolism for key flavonoid fractions. But the usual caution applies: cell culture and rodent models are starting points, not endpoints. The gap between in vitro GABA binding affinity and a measurable clinical outcome in a human being is wide.

No therapeutic claims can be made on the current evidence. What can be said is that the research questions are legitimate and the chemistry gives researchers a mechanistic rationale to keep asking them.

Regulatory status in Australia

Passiflora incarnata aerial parts are not scheduled under the current Poisons Standard (the document that classifies medicines as Schedule 2 through to Schedule 9 in Australia). Products containing passionflower extracts can be listed on the Australian Register of Therapeutic Goods (ARTG) as listed medicines (AUST L), which means the TGA accepts the ingredients as generally low-risk but does not evaluate the specific product for efficacy. Listed medicines can carry only permitted indications, a tightly defined set of low-level claims such as "traditionally used to support healthy sleep" or "mild nervine tonic." They cannot carry claims about treating, preventing or curing any diagnosed condition.

If a sponsor wants to make higher-level therapeutic claims, the product must be registered (AUST R), which requires submission of clinical evidence. Most passionflower products on Australian shelves sit in the ARTG listed category, which tells you something about the state of the evidence base.

Good Manufacturing Practice (GMP) compliance is required for all listed and registered medicines in Australia regardless of how mild the ingredient profile appears.

For comparison: kava (Piper methysticum) occupies a notably different regulatory position; kava imports for personal use have historically been subject to permit requirements and quantity limits under the Customs (Prohibited Imports) Regulations 1956, reflecting a different risk profile driven by hepatotoxicity concerns (under specific conditions of use) and a more restricted evidence history. Passionflower does not carry that import restriction, though products must still comply with TGA requirements to be supplied as medicines.

The β-carboline alkaloids in passionflower are worth one further regulatory note. Harmaline and harmine appear in Schedule 9 of the Poisons Standard at certain concentrations and in isolated form, as they are associated with MAO-inhibiting activity and psychoactive potential. Products containing the whole plant in typical herbal doses are not captured by that scheduling, but isolated alkaloid fractions would be a different matter. This is one of those areas where the herbal preparation versus isolated constituent distinction genuinely matters from a regulatory standpoint.

How passionflower fits in the broader botanical picture

Part of what I find genuinely interesting about P. incarnata is how it sits at the intersection of multiple active research areas. The flavonoid-GABA connection draws interest from researchers also studying kava kavalactones and valerian valerenic acid. The β-carboline fraction places it in unexpected proximity (chemically, if not practically) to discussions about harmala alkaloids in contexts far beyond herbal teas. And the general question of how complex botanical mixtures behave differently from isolated constituents echoes discussions in cannabis research about the entourage effect, the idea that the whole plant matrix may behave differently from any single compound extracted from it. That concept isn't exclusive to cannabinoid research; it's a live question across phytomedicine broadly.

The vine my nan grew still climbs a fence somewhere in the Hills, I imagine. I have no idea if she had any of this chemistry in mind. She probably didn't. But the fact that researchers are still working through these questions, more carefully than the old herbals ever did; feels right to me.

Sources

, Naomi Ellison, Botanical & phytomedicine writer

Common questions

Is passionflower a scheduled substance in Australia?: Passiflora incarnata aerial parts are not scheduled under Australia's Poisons Standard, meaning they can be sold in listed complementary medicines (AUST L) on the ARTG without a prescription. However, isolated β-carboline alkaloids from the plant — such as harmine and harmaline — do appear in Schedule 9 at certain concentrations and in isolated form, so the whole-plant versus isolated-constituent distinction matters legally.
What are the main chemical constituents researchers have focused on?: The most studied constituents in Passiflora incarnata are the C-glycosyl flavonoids — particularly vitexin, isovitexin, orientin and chrysin — and the harmane β-carboline alkaloids (harman, harmine, harmaline). Chrysin has been examined for GABA-A receptor binding affinity in laboratory models, while the β-carbolines are known MAO inhibitors at sufficient concentration. The relative contribution of each fraction to any observed effects in human studies has not been definitively established.
What does an AUST L listing mean for a passionflower product?: An AUST L listing on the Australian Register of Therapeutic Goods (ARTG) means the TGA has accepted the ingredients as generally low-risk for the listed use, but has not evaluated that specific product for clinical efficacy. Listed passionflower products may carry only the TGA's permitted low-level indications — such as 'traditionally used as a mild nervine tonic' — and may not make claims about treating, preventing or curing any named medical condition.
Are there any known interaction concerns with passionflower?: The β-carboline alkaloids present in Passiflora incarnata have monoamine oxidase inhibitory (MAOI) properties at sufficient concentration, which is a potential pharmacological interaction point with prescription MAOIs and serotonergic medicines. Anyone taking pharmaceutical medicines should consult a registered pharmacist or medical practitioner before using passionflower preparations. This article does not constitute medical advice.
How does passionflower research compare to other nervine botanicals like kava?: The human clinical trial database for Passiflora incarnata is small — most trials involve fewer than 50 participants and short follow-up periods. Kava (Piper methysticum) has a larger, though still debated, clinical dataset, but carries a different regulatory status in Australia, including import permit requirements for personal use and specific hepatotoxicity warnings. Both plants sit in a category where ethnobotanical history is strong but high-quality clinical evidence remains limited.