Compound Monograph
Chalepensin
Chalepensin is rue's prenylated furanocoumarin — the isolated antifertility principle behind the plant's abortifacient reputation, and a mechanism-based inhibitor of CYP2A6, CYP1A1 and CYP3A4 that destroys the enzyme it is metabolised by. It is also the most potent anthelmintic compound rue makes.
Sources · 4
Where Does It Come From?
Chalepensin is a naturally occurring furanocoumarin (3-prenylated psoralen; 3-(1,1-dimethylallyl)psoralen), found in Rue and 3 other sources. It is flagged as toxic.
Concentration
Content by Source
Concentrations not reported. No percent-dry-weight or mg/g figures have been published for this compound in its source plants.
Chalepensin at a Glance
Chalepensin is a furanocoumarin carrying a five-carbon prenyl group at position 3 — structurally, 3-(1,1-dimethylallyl)psoralen. It is named for Ruta chalepensis, the fringed rue it was first drawn from, and its distribution appears confined to the Rutaceae 6Reference 6ReviewChalepin and chalepensin: occurrence, biosynthesis and therapeutic potential — reviewView study →.
Two things make it consequential. It is the isolated antifertility principle of rue: fractionating chloroform extracts of root, stem and leaf against a rat post-coital model led to chalepensin as the active component, acting at the earliest stages of pregnancy — and with some toxicity of its own 1Reference 1AnimalAntifertility principle of Ruta graveolens — animal modelView study →. And it is a mechanism-based inhibitor of several cytochrome P450 enzymes, meaning the enzyme metabolises it into a reactive epoxide that then destroys the enzyme 3,
Alongside that, it is the most potent anthelmintic molecule rue is known to make, with a selectivity index against Trichinella spiralis larvae in the thousands 8Reference 8In vitroAntiparasitic efficacy of chalepensin from Ruta chalepensis L. against Trichinella spiralis: in vitro, in vivo, and molecular docking study — animal modelView study →.
The Prenyl Group Changes What It Does to DNA
Chalepensin is a psoralen with one addition, and the addition matters. Plain psoralen, bergapten and xanthotoxin are the molecules behind rue’s blistering phototoxicity and behind clinical PUVA therapy: under UV-A they react at both the furan and the pyrone double bonds, forming a monoadduct with one DNA strand and then a crosslink joining both strands. The interstrand crosslink is what makes a psoralen a potent photosensitiser.
Chalepensin’s 3-prenyl substituent sits on the pyrone ring and blocks that second reaction. When it was tested for DNA photobinding under its systematic name, 3-(α,α-dimethylallyl)psoralen was found to form mainly 4′,5′-monofunctional adducts — furan-side monoadducts, without the bifunctional crosslinking that defines the class 7Reference 7In vitroVedaldi D, Dall’Acqua F, Caffieri S, Rodighiero G (1979). 3-(α,α-Dimethylallyl)-psoralen: a linear furocoumarin forming mainly 4′,5′-monofunctional adducts with DNA — in vitro. Photochemistry and Photobiology. https://pubmed.ncbi.nlm.nih.gov/482377/View study →. It is the same principle that makes rue’s furoquinoline alkaloids (skimmianine, dictamnine) milder photosensitisers than its furanocoumarins, arrived at by a different structural route.
This is not a safety clearance. A monoadduct is still a covalent lesion in DNA, and chalepensin is also photochemically unstable — it isomerises under light to the coumarin rutolide (clausindin) 12Reference 12In vitroPhotoisomerization of chalepensin to rutolide (clausindin) — in vitroView study →. But it does mean chalepensin should not be assumed to carry bergapten’s photosensitising potency simply because it is a furanocoumarin from the same plant.
What It's Used For
The literature splits cleanly into three strands that have almost nothing to do with one another: reproductive toxicology from the late 1980s, a sustained programme of drug-metabolism work from Taiwan in 2011–2013, and a recent Mexican–Spanish antiparasitic and antitumour series.
The finding that gives rue’s abortifacient reputation a molecule. Chloroform extracts of Ruta graveolens root, stem and leaf given intragastrically to rats on days 1–10 post-coitum produced significant antifertility activity; fractionation identified chalepensin as the active component, “with some toxicity”, and time-dosing experiments showed it acts at the early stages of pregnancy — implantation rather than late gestation. The authors were explicit that they could not tell whether the antifertility effect was a direct action or a manifestation of the compound’s toxicity 1Reference 1AnimalAntifertility principle of Ruta graveolens — animal modelView study →.
Gap: one 1989 study, in rats, with the mechanism unresolved and the compound’s own toxicity confounding it. A separate 1991 study of R. graveolens post-coital activity tested whole-plant preparations rather than chalepensin, found them active in rats but inactive in hamsters, and found rutin inactive 2Reference 2AnimalPost-coital antifertility action of Ruta graveolens in female rats and hamsters — animal modelView study → — so the species-generality of the effect is not established, and it belongs to the plant in that study, not to this molecule.
The best-characterised of chalepensin’s actions, and the one with real interaction implications. Chalepensin is both a substrate and a mechanism-based inhibitor of human CYP2A6: pre-incubation with NADPH dropped its IC50 by 98%, the inactivation was time-dependent (kinact 0.044 min⁻¹, KI 2.64 µM), spectrally detectable P450 was lost, and LC/MS identified an unstable epoxide intermediate — trapped as the dihydrodiol and as a glutathione conjugate — as the likely destructive species. The variants CYP2A6*7 and *10 were less susceptible 3Reference 3In vitroMechanism-based inhibition of cytochrome P450 (CYP)2A6 by chalepensin in recombinant systems, in human liver microsomes and in mice in vivo — in vitro and animal modelView study →.
A follow-up screened the wider panel: CYP1A1 and CYP3A4 underwent pronounced mechanism-based inactivation, not fully recoverable by dialysis, while CYP2E1 was least affected. The enzymes most susceptible were the ones with the highest epoxidation activity, which ties the mechanism together 4Reference 4In vitroMechanism-based inhibition of CYP1A1 and CYP3A4 by the furanocoumarin chalepensin — in vitroView study →. In mice, 10 mg/kg orally for seven days lowered hepatic Cyp2a activity while raising immunodetected Cyp2a5 protein — suicide-inhibited enzyme is protected from degradation — and simultaneously induced Cyp2b through activation of the constitutive androstane receptor 5Reference 5AnimalA dual function of the furanocoumarin chalepensin in inhibiting Cyp2a and inducing Cyp2b in mice: the protein stabilization and receptor-mediated activation — animal modelView study →.
Gap: all in vitro or in mice; no human interaction study exists, and no one has measured what plasma concentration of chalepensin a rue preparation produces, so the threshold estimates cannot be translated into a real-world risk.
The strongest recent work. Against Trichinella spiralis first-stage larvae, chalepensin isolated from R. chalepensis gave an LC50 of 0.1 µg/mL with a selectivity index of 8,561 against Vero cells — far better than graveoline (LC50 1.1 µg/mL, SI 162) or the parent extract (LC50 28.2 µg/mL, SI 22.4). In mice, 50 mg/kg/day for three days cut larval burden by 90.7% when given during the intestinal phase, but only ~37% against migrating or encysted larvae; docking suggested thymidylate synthase as a target 8Reference 8In vitroAntiparasitic efficacy of chalepensin from Ruta chalepensis L. against Trichinella spiralis: in vitro, in vivo, and molecular docking study — animal modelView study →.
Against Strongyloides venezuelensis it gave LC50 3.9 µg/mL (SI 990) on infective larvae and 16.8 µg/mL (SI 200) on adult females, with scanning electron microscopy showing protuberances across the parasite body 9Reference 9In vitroAntiparasitic activity of chalepensin and graveoline isolated from Ruta chalepensis L.: in vitro evaluation against Strongyloides venezuelensis — in vitroView study →.
Gap: a compound with an antifertility action and mechanism-based P450 inhibition is not a plausible human anthelmintic whatever its selectivity index; and the stage-dependence — nine-tenths of the effect confined to the intestinal phase — limits it even as a lead.
Chalepensin was cytotoxic to L5178Y-R murine lymphoma cells (IC50 8.1 µg/mL, SI 66.5), reduced tumour volume in tumour-bearing BALB/c mice between days 10 and 20, and prolonged survival comparably to vincristine under the conditions tested. Intraperitoneal doses of 100 and 1,000 mg/kg produced no mortality and no significant haematological or biochemical change in an acute-toxicity arm, and docking suggested interaction with the cyclin A2–CDK2 complex 10Reference 10AnimalPharmacological potential of chalepensin from Ruta chalepensis L.: acute toxicity and in vivo antitumor activity in the L5178Y-R murine model — animal modelView study →.
Gap: a single 2026 study in one syngeneic model. The reassuring acute-toxicity result is a single-dose observation and says nothing about repeat dosing, and nothing about reproductive toxicity, which is where this molecule’s known harm sits.
In the first report of anti-MRSA activity from R. chalepensis, chalepensin was one of two most active of nineteen isolated compounds, active against four of six strains tested, with MICs in the 32–128 µg/mL range across a panel including the Kuwaiti efflux-pump isolate XU212 and EMRSA-15 11Reference 11In vitroAnti-MRSA constituents from Ruta chalepensis (Rutaceae) grown in Iraq, and in silico studies on two of most active compounds, chalepensin and 6-hydroxy-rutin 3′,7-dimethyl ether — in vitroView study →.
Gap: MICs in the tens-of-micrograms range are weak by antibiotic standards — the norfloxacin comparator ran at 16 µg/mL — and this is a screening result with no in-vivo follow-up.
R. chalepensis was among the more active of 32 plants screened against Entamoeba histolytica trophozoites in a survey of northeast Mexican traditional medicine, with chalepensin among the compounds isolated from the active extract 13Reference 13In vitroAntiprotozoal activity against Entamoeba histolytica of plants used in northeast Mexican traditional medicine: bioactive compounds from Lippia graveolens and Ruta chalepensis — in vitroView study →. The 2021 review lists antiprotozoal activity among the class properties of the 3-prenylated coumarins 6Reference 6ReviewChalepin and chalepensin: occurrence, biosynthesis and therapeutic potential — reviewView study →.
Gap: screening level, with the compound’s individual contribution to the extract’s activity not separated out.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| CYP2A6 (and CYP1A1, CYP3A4) | epoxidation → reactive intermediate → irreversible enzyme inactivation | drug interactions |
| Constitutive androstane receptor (CAR) | activation → Cyp2b induction in mice | drug interactions |
| Early pregnancy / implantation | anti-implantation in rats; mechanism unresolved | antifertility |
| Nematode thymidylate synthase (predicted) | docking affinity; cuticle disruption observed | anthelmintic |
| Cyclin A2–CDK2 (predicted) | docking affinity consistent with a cytostatic effect | antitumour |
| DNA, on UV-A activation | 4′,5′-monofunctional adducts; no interstrand crosslink | photochemistry |
Pharmacokinetics
Poorly characterised, but the metabolic route is known and it is the interesting part. Chalepensin is epoxidised on the furan ring by the same P450s it inhibits; the epoxide is unstable, is detected as the corresponding dihydrodiol, and is conjugated with glutathione — glutathione conjugation reduced the inactivation of CYP2A6 and protected CYP3A4, so cellular thiol status modulates its own toxicity 3,
What is missing is everything quantitative in a mammal: no absorption figure, no bioavailability, no half-life, no human data. And critically, no one has measured what concentration of chalepensin a rue tea or tincture delivers, which is the number that would tell you whether the enzyme-inactivation thresholds are ever reached in practice.
Clinical Trials
None, and none should be expected. There are no clinical trials of chalepensin for any indication.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| None | — | — | Antifertility, P450, anthelmintic, antitumour |
Last checked: September 2026.
Isolate vs. Plant Studies
The isolate question is unusually clean here: nearly every result cited is purified chalepensin, isolated from R. chalepensis or R. graveolens and tested on its own 1,
The transfer problem runs the other way. Rue is a low-dose herb whose internal use is discouraged, its chalepensin content varies with species, chemotype, plant part and season, and nothing standardises a preparation to this compound. So the isolate work establishes what the molecule does, and establishes nothing about the exposure anyone actually receives. Note too that a substantial slice of the antiparasitic and antibacterial literature is R. chalepensis, not R. graveolens — related species with overlapping but not identical chemistry, and worth keeping straight when reading rue’s phytochemistry.
Its Role in Plants
Chalepensin belongs to the prenylated coumarins, built by attaching a five-carbon isoprene unit to a coumarin scaffold; it and its dihydrofuran relative chalepin are the pair that defines this chemistry in Ruta, and their biosynthesis and restricted Rutaceae distribution were reviewed together in 2021 6Reference 6ReviewChalepin and chalepensin: occurrence, biosynthesis and therapeutic potential — reviewView study →. The prenyl group raises lipophilicity, which is the usual explanation for why prenylated coumarins are more membrane-active — and therefore more antimicrobial and more insecticidal — than their unsubstituted parents.
Its activity profile across nematodes, protozoa and bacteria 8,
Prevalence in Nature
Chalepensin is a genus Ruta compound with a narrow reach beyond it. It was first isolated from Ruta chalepensis and takes its name from that species; it is also reported from R. graveolens, R. angustifolia, and from Boenninghausenia and Clausena — with distribution restricted to the Rutaceae as far as the 2021 review could establish 6Reference 6ReviewChalepin and chalepensin: occurrence, biosynthesis and therapeutic potential — reviewView study →. It has additionally been reported from Dorstenia foetida and from the Yucatán tree Stauranthus perforatus, both furanocoumarin-rich plants.
Within rue, it is present in leaf, stem and root — the antifertility fractionation drew on all three 1Reference 1AnimalAntifertility principle of Ruta graveolens — animal modelView study →, and the recent antiparasitic isolations used leaves and stems 8Reference 8In vitroAntiparasitic efficacy of chalepensin from Ruta chalepensis L. against Trichinella spiralis: in vitro, in vivo, and molecular docking study — animal modelView study →. No reliable percentage figure for chalepensin content in field-grown rue was found, so no per-source comparison can be drawn; the general pattern for the plant is that furanocoumarins concentrate in the aerial parts while the acridone alkaloids sit in the roots, and that yield varies strongly with chemotype and provenance.
Discovery & Synthesis
Chalepensin was first isolated from Ruta chalepensis, which is where its name comes from, and was characterised alongside chalepin, the dihydrofuranocoumarin that shares its 3-prenyl substitution 6Reference 6ReviewChalepin and chalepensin: occurrence, biosynthesis and therapeutic potential — reviewView study →. Its photoisomerisation to rutolide (clausindin) was described in 1975 12Reference 12In vitroPhotoisomerization of chalepensin to rutolide (clausindin) — in vitroView study → — an early demonstration that this molecule is not stable to light, which is worth knowing when interpreting phytochemical analyses of dried or sun-exposed plant material.
Biosynthetically it is a coumarin with an isoprene unit attached at C-3; the plausible route was worked out in the 2021 review 6Reference 6ReviewChalepin and chalepensin: occurrence, biosynthesis and therapeutic potential — reviewView study →. There is no commercial production: it is isolated in milligram quantities from Ruta for research, and is not manufactured.
Patents: not yet researched (future patent-loop pass).
Toxicity & Safety
Chalepensin is flagged toxic, and the flag rests on two independent grounds rather than on acute lethality — for which, in a single-dose mouse study, it showed none at 1,000 mg/kg 10Reference 10AnimalPharmacological potential of chalepensin from Ruta chalepensis L.: acute toxicity and in vivo antitumor activity in the L5178Y-R murine model — animal modelView study →.
- Antifertility in pregnancy. It is the isolated compound behind rue’s abortifacient reputation, acting at the earliest stage of pregnancy in rats 1Reference 1AnimalAntifertility principle of Ruta graveolens — animal modelView study →. Nothing about that finding is reassuring at any dose.
- Mechanism-based P450 inactivation. It permanently disables CYP2A6, CYP1A1 and CYP3A4 by being metabolised into a reactive epoxide 3,
4Reference 3In vitroMechanism-based inhibition of cytochrome P450 (CYP)2A6 by chalepensin in recombinant systems, in human liver microsomes and in mice in vivo — in vitro and animal modelView study →Reference 4In vitroMechanism-based inhibition of CYP1A1 and CYP3A4 by the furanocoumarin chalepensin — in vitroView study → . CYP3A4 handles a very large share of prescribed medicines. - A photoreactive furanocoumarin. It forms monoadducts with DNA under UV-A 7Reference 7In vitroVedaldi D, Dall’Acqua F, Caffieri S, Rodighiero G (1979). 3-(α,α-Dimethylallyl)-psoralen: a linear furocoumarin forming mainly 4′,5′-monofunctional adducts with DNA — in vitro. Photochemistry and Photobiology. https://pubmed.ncbi.nlm.nih.gov/482377/View study → — weaker than a crosslinking psoralen, but not inert.
- No human data at all. Every figure here is animal or in vitro, and no rue preparation is standardised to this compound.
Full Safety & Interactions Detail
Reproductive. The antifertility result is the defining safety fact. Chalepensin was isolated as the compound responsible for an anti-implantation effect in rats, acting in the first days after coitus, and the isolating authors recorded that it carried “some toxicity” and that the two could not be separated 1Reference 1AnimalAntifertility principle of Ruta graveolens — animal modelView study →. This is the molecular counterpart of rue’s traditional and documented status as an abortifacient, and it is why the herb is contraindicated in pregnancy. The related 1991 study should not be cited as confirmation for the isolate: it tested plant preparations, found them active in rats and inactive in hamsters, and included no chalepensin arm 2Reference 2AnimalPost-coital antifertility action of Ruta graveolens in female rats and hamsters — animal modelView study →.
Interactions — the practical hazard. Mechanism-based inhibition differs from ordinary competitive inhibition in a way that matters: the enzyme is destroyed rather than occupied, so activity returns only as new enzyme is synthesised, over days rather than hours. Chalepensin does this to CYP3A4 4Reference 4In vitroMechanism-based inhibition of CYP1A1 and CYP3A4 by the furanocoumarin chalepensin — in vitroView study →, the enzyme responsible for metabolising a large fraction of prescription drugs, and to CYP2A6 3Reference 3In vitroMechanism-based inhibition of cytochrome P450 (CYP)2A6 by chalepensin in recombinant systems, in human liver microsomes and in mice in vivo — in vitro and animal modelView study → and CYP1A1 4Reference 4In vitroMechanism-based inhibition of CYP1A1 and CYP3A4 by the furanocoumarin chalepensin — in vitroView study →. In mice it also induces Cyp2b by activating CAR 5Reference 5AnimalA dual function of the furanocoumarin chalepensin in inhibiting Cyp2a and inducing Cyp2b in mice: the protein stabilization and receptor-mediated activation — animal modelView study →, so the net effect on a co-administered drug depends on which enzyme clears it. Rue’s co-occurring furanocoumarins, bergapten and xanthotoxin, are themselves established CYP3A4 inhibitors — the same chemistry that makes grapefruit juice a drug-interaction problem — so the plant presents several inhibitors at once. Assume a genuine interaction risk and no data with which to size it.
Photochemistry. Chalepensin forms mainly 4′,5′-monofunctional adducts with DNA rather than the interstrand crosslinks its unsubstituted relatives make 7Reference 7In vitroVedaldi D, Dall’Acqua F, Caffieri S, Rodighiero G (1979). 3-(α,α-Dimethylallyl)-psoralen: a linear furocoumarin forming mainly 4′,5′-monofunctional adducts with DNA — in vitro. Photochemistry and Photobiology. https://pubmed.ncbi.nlm.nih.gov/482377/View study →, and rue’s photomutagenicity in the standard assay is dominated by bergapten rather than by the prenylated coumarins. Treat it as a contributor to rue’s phototoxicity, not the principal cause.
Scope. No repeat-dose toxicology, no genotoxicity panel, no carcinogenicity data and no human safety data exist for chalepensin. The one acute-toxicity study is a single intraperitoneal dose in mice 10Reference 10AnimalPharmacological potential of chalepensin from Ruta chalepensis L.: acute toxicity and in vivo antitumor activity in the L5178Y-R murine model — animal modelView study →, and its clean result should not be generalised.
Dosage
There is no human dose for chalepensin and there should not be one — an antifertility compound that irreversibly inactivates CYP3A4 is not a candidate for self-administration. The figures below are experimental, recorded for scale only.
| Setting | Route | Dose or concentration |
|---|---|---|
| Rat post-coital antifertility 1Reference 1AnimalAntifertility principle of Ruta graveolens — animal modelView study → | intragastric, days 1–10 | active fraction of a chloroform extract |
| Mouse hepatic Cyp2a suppression 5Reference 5AnimalA dual function of the furanocoumarin chalepensin in inhibiting Cyp2a and inducing Cyp2b in mice: the protein stabilization and receptor-mediated activation — animal modelView study → | oral, 7 days | 10 mg/kg/day |
| Mouse trichinellosis 8Reference 8In vitroAntiparasitic efficacy of chalepensin from Ruta chalepensis L. against Trichinella spiralis: in vitro, in vivo, and molecular docking study — animal modelView study → | oral, 3 days | 50 mg/kg/day |
| Mouse lymphoma, acute-toxicity arm 10Reference 10AnimalPharmacological potential of chalepensin from Ruta chalepensis L.: acute toxicity and in vivo antitumor activity in the L5178Y-R murine model — animal modelView study → | intraperitoneal | 100 and 1,000 mg/kg, single dose |
| CYP2A6 inactivation 3Reference 3In vitroMechanism-based inhibition of cytochrome P450 (CYP)2A6 by chalepensin in recombinant systems, in human liver microsomes and in mice in vivo — in vitro and animal modelView study → | enzyme assay | KI 2.64 µM |
| T. spiralis L1 larvae 8Reference 8In vitroAntiparasitic efficacy of chalepensin from Ruta chalepensis L. against Trichinella spiralis: in vitro, in vivo, and molecular docking study — animal modelView study → | culture | LC50 0.1 µg/mL |
| MRSA panel 11Reference 11In vitroAnti-MRSA constituents from Ruta chalepensis (Rutaceae) grown in Iraq, and in silico studies on two of most active compounds, chalepensin and 6-hydroxy-rutin 3′,7-dimethyl ether — in vitroView study → | culture | MIC 32–128 µg/mL |
These are doses studied in research and are not a personal recommendation.
References
- Kong YC, Lau CP, Wat KH, et al. (1989). Antifertility principle of Ruta graveolens — animal model. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/2748734/
- Gandhi M, Lal R, Sankaranarayanan A, Sharma PL (1991). Post-coital antifertility action of Ruta graveolens in female rats and hamsters — animal model. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/1753787/
- Ueng YF, Chen CC, Chung YT, et al. (2011). Mechanism-based inhibition of cytochrome P450 (CYP)2A6 by chalepensin in recombinant systems, in human liver microsomes and in mice in vivo — in vitro and animal model. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/21418183/
- Ueng YF, Chen CC, Yamazaki H, et al. (2013). Mechanism-based inhibition of CYP1A1 and CYP3A4 by the furanocoumarin chalepensin — in vitro. Drug Metabolism and Pharmacokinetics. https://pubmed.ncbi.nlm.nih.gov/23257392/
- Lo WS, Lim YP, Chen CC, et al. (2012). A dual function of the furanocoumarin chalepensin in inhibiting Cyp2a and inducing Cyp2b in mice: the protein stabilization and receptor-mediated activation — animal model. Archives of Toxicology. https://pubmed.ncbi.nlm.nih.gov/22790670/
- Nahar L, Al-Majmaie S, Al-Groshi A, Rasul A, Sarker SD (2021). Chalepin and chalepensin: occurrence, biosynthesis and therapeutic potential — review. Molecules. https://pubmed.ncbi.nlm.nih.gov/33799365/
- Vedaldi D, Dall’Acqua F, Caffieri S, Rodighiero G (1979). 3-(α,α-Dimethylallyl)-psoralen: a linear furocoumarin forming mainly 4′,5′-monofunctional adducts with DNA — in vitro. Photochemistry and Photobiology. https://pubmed.ncbi.nlm.nih.gov/482377/
- Rodríguez-Garza NE, Marín M, Sánchez-Montejo J, et al. (2025). Antiparasitic efficacy of chalepensin from Ruta chalepensis L. against Trichinella spiralis: in vitro, in vivo, and molecular docking study — animal model. Acta Tropica. https://pubmed.ncbi.nlm.nih.gov/41338405/
- Rodríguez-Garza NE, Marín M, Sánchez-Montejo J, et al. (2025). Antiparasitic activity of chalepensin and graveoline isolated from Ruta chalepensis L.: in vitro evaluation against Strongyloides venezuelensis — in vitro. Pathogens. https://pubmed.ncbi.nlm.nih.gov/40430740/
- Rodríguez-Garza NE, Quintanilla-Licea R, Caballero-Hernández DE, et al. (2026). Pharmacological potential of chalepensin from Ruta chalepensis L.: acute toxicity and in vivo antitumor activity in the L5178Y-R murine model — animal model. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/41654069/
- Al-Majmaie S, Nahar L, Rahman MM, et al. (2021). Anti-MRSA constituents from Ruta chalepensis (Rutaceae) grown in Iraq, and in silico studies on two of most active compounds, chalepensin and 6-hydroxy-rutin 3′,7-dimethyl ether — in vitro. Molecules. https://pubmed.ncbi.nlm.nih.gov/33669881/
- Reisch J, Szendrei K (1975). Photoisomerization of chalepensin to rutolide (clausindin) — in vitro. Archiv der Pharmazie. https://pubmed.ncbi.nlm.nih.gov/1221980/
- Quintanilla-Licea R, Mata-Cárdenas BD, Vargas-Villarreal J, et al. (2014). Antiprotozoal activity against Entamoeba histolytica of plants used in northeast Mexican traditional medicine: bioactive compounds from Lippia graveolens and Ruta chalepensis — in vitro. Molecules. https://pubmed.ncbi.nlm.nih.gov/25517343/
