# Cascarilla (Cinchona officinalis)

**Canonical URL:** https://ingredients.hermeticasuperfoods.com/ingredients/cascarilla-cinchona-officinalis
**Data Source:** Hermetica Superfoods Ingredient Encyclopedia
**Updated:** 2026-04-02
**Evidence Score:** 1 / 10
**Category:** South American
**Also Known As:** Cinchona officinalis, Peruvian bark, Jesuit's bark, quina, quinquina, fever bark, red cinchona

## Overview

Cinchona officinalis bark contains quinoline alkaloids—primarily quinine, quinidine, cinchonine, and cinchonidine—that exert antimalarial activity by inhibiting heme polymerization within Plasmodium parasites and exhibit [anti-inflammatory](/ingredients/condition/inflammation) effects through NF-κB pathway suppression. Preclinical data show total alkaloid concentrations of 4–16% by bark weight, ethyl acetate fractions demonstrate DPPH [antioxidant](/ingredients/condition/antioxidant) IC50 values as low as 17.63 μg/mL, and methanol bark extracts produce 17–57% anti-inflammatory inhibition compared to diclofenac controls, though large-scale human RCTs for supplemental use remain absent.

## Health Benefits

- **Antimalarial Activity**: Quinine and quinidine inhibit heme polymerization in Plasmodium falciparum by interacting with the quinuclidine ring's active nitrogen, preventing the parasite from detoxifying toxic free heme and forming hemozoin crystals, ultimately killing the parasite.
- **Antipyretic and Febrifuge Effects**: Historically documented as a febrifuge, cinchona alkaloids reduce fever through central and peripheral thermoregulatory mechanisms; quinine and quinidine demonstrate equivalent febrifugal potency, while cinchonine and cinchonidine are comparatively less potent.
- **[Antioxidant Protection](/ingredients/condition/antioxidant)**: Ethyl acetate and water-insoluble bark fractions exhibit strong DPPH free-radical scavenging with IC50 values of 23.57 μg/mL and 17.63 μg/mL respectively, indicating high antioxidant potential driven by polyphenols, phenolic acids, and flavonoids present in the bark.
- **Anti-Inflammatory Action**: Polyphenolic compounds and alkaloids in bark extracts suppress the NF-κB signaling pathway in lipopolysaccharide-stimulated cells, reducing [pro-inflammatory cytokine](/ingredients/condition/inflammation) production; methanol extracts showed 17.0–57.3% anti-inflammatory inhibition in vitro.
- **Anti-Arthritic Potential**: Bark extracts inhibited albumin denaturation—a proxy for anti-arthritic activity—by 18.4–58.5% at concentrations up to 75 mg/mL in preclinical assays, comparable in trend to diclofenac controls, suggesting joint-protective mechanisms via protein stabilization.
- **Anticancer Research Interest**: Quinine-loaded iron oxide nanoparticles demonstrated enhanced cytotoxicity and apoptosis induction in MCF-7 breast cancer cells compared to free extract, attributed to improved intracellular bioavailability and alkaloid stabilization in nanoparticle form.
- **[Cardiovascular](/ingredients/condition/heart-health) Antiarrhythmic Activity**: Quinidine, a stereoisomer of quinine found in cinchona bark, is a well-established Class Ia antiarrhythmic agent that blocks cardiac sodium channels and prolongs the action potential, and has been used clinically for atrial fibrillation and ventricular arrhythmias.

## Mechanism of Action

Quinoline alkaloids in Cinchona officinalis—quinine, quinidine, cinchonine, and cinchonidine—share a structurally active quinuclidine ring with a basic nitrogen center and a methylene alcohol group that intercalates with heme in Plasmodium-infected erythrocytes, blocking the conversion of toxic ferriprotoporphyrin IX into inert hemozoin crystals and causing oxidative parasite death. [Anti-inflammatory](/ingredients/condition/inflammation) activity is mediated by polyphenols and alkaloids that inhibit NF-κB nuclear translocation in macrophages stimulated with lipopolysaccharide, thereby reducing transcription of pro-inflammatory genes encoding TNF-α, IL-1β, and IL-6. Antioxidant mechanisms involve direct hydrogen-atom donation from phenolic hydroxyl groups—particularly from tannins, phenolic acids, and flavonoids such as 2,4-di-tert-butylphenol (12.24%) and 2(1H)-quinolinone (11.95%)—to quench DPPH and [reactive oxygen species](/ingredients/condition/antioxidant). Quinidine exerts antiarrhythmic effects by blocking fast inward sodium channels (INa) and outward potassium channels (IKr) in cardiomyocytes, prolonging the QRS complex and QT interval and suppressing ectopic pacemaker activity.

## Clinical Summary

No modern randomized controlled trials specifically evaluating Cinchona officinalis bark extract as a standardized supplement with defined doses and human endpoints have been identified. The strongest clinical evidence is for isolated quinine as a pharmaceutical antimalarial agent, where its efficacy against Plasmodium falciparum is historically and pharmacologically established, though it is administered under medical supervision at doses carrying significant risk of cinchonism. Preclinical [anti-inflammatory](/ingredients/condition/inflammation) and [antioxidant](/ingredients/condition/antioxidant) outcomes are promising but lack translation to human effect sizes, confidence intervals, or validated biomarker endpoints. The anticancer nanoparticle data are early-stage with no human studies, and the overall evidence base for supplemental use remains at the preliminary preclinical tier.

## Nutritional Profile

Cinchona officinalis bark is not a significant source of macronutrients and is consumed medicinally rather than nutritionally. Primary bioactives are quinoline alkaloids totaling 4–16% of dry bark weight: quinine (predominant in C. ledgeriana), quinidine, cinchonidine, and cinchonine in varying ratios by species. Secondary phytochemicals include tannins (approximately 3–10%), saponins, steroids, terpenoids, phenolic acids, flavonoids, and glycosides; aqueous stem bark extracts yield total phenolics of approximately 0.548 mg/100 mg dry weight. GC-MS analysis of methanol extracts identifies additional compounds including phthalic acid, hexadecanoic acid (palmitic acid), 9,12-octadecadienoic acid (linoleic acid), heptadecanoic acid, γ-sitosterol, phenol, and cinchonab-9-one. Bioavailability of alkaloids is enhanced significantly in nanoparticle formulations compared to crude aqueous extracts; ethanol-based extraction yields superior alkaloid recovery relative to water extraction alone.

## Dosage & Preparation

- **Bark Decoction (Traditional)**: 1–3 grams of dried powdered bark steeped in 200 mL boiling water for 10–15 minutes; consumed 1–2 times daily as a febrifuge or digestive bitter; no modern standardized dose established.
- **Methanol/Ethanol Extract**: Prepared via Soxhlet extraction or maceration; yields highest total alkaloid concentrations (up to 16% quinine by weight); used in research settings but not standardized for consumer supplementation.
- **Aqueous Extract**: Total phenolics reported at 0.548 mg/100 mg dry weight; lower alkaloid yield than methanol extraction but considered safer for oral preparations.
- **Standardized Bark Powder**: Historically standardized to 4–16% total quinoline alkaloids depending on Cinchona species; commercial pharmaceutical quinine sulfate is isolated and dosed at 324–648 mg per dose for malaria treatment under medical prescription.
- **Nanoparticle Formulations (Experimental)**: Green-synthesized iron oxide nanoparticles using FeCl3 (0.05–0.1 M) with bark extract (50–100 mg) enhance intracellular alkaloid bioavailability; strictly experimental with no approved human dosing protocol.
- **Tonic Water (Low-Dose Quinine)**: Commercially available beverages contain trace quinine (up to 83 mg/L in the EU); insufficient for therapeutic effect but responsible for characteristic bitterness.
- **Important Note**: Supplemental self-dosing of cinchona bark is not recommended without medical oversight due to narrow therapeutic index of quinoline alkaloids.

## Safety & Drug Interactions

Cinchona alkaloids at antimalarial pharmaceutical doses cause a well-characterized syndrome called cinchonism, characterized by tinnitus, headache, nausea, vomiting, visual disturbances, and vertigo; these effects are dose-dependent and reversible upon cessation, but high doses can cause severe hypoglycemia, hemolytic anemia, thrombocytopenia, and cardiac arrhythmias. Quinidine carries a significant risk of QT interval prolongation and potentially fatal ventricular arrhythmias (torsades de pointes), and should never be combined with other QT-prolonging drugs including certain antiarrhythmics, fluoroquinolone antibiotics, macrolides, and antipsychotics without cardiac monitoring. Cinchona bark and isolated quinine are contraindicated in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency due to risk of hemolysis, in patients with myasthenia gravis, optic neuritis, tinnitus, or hypersensitivity to quinoline alkaloids, and in pregnancy (quinine is teratogenic at high doses and has been associated with congenital defects and premature labor). Preclinical data show cytotoxicity to insect Sf9 and mammalian CHO cell lines from certain bark compounds, reinforcing caution; no established maximum safe supplemental dose exists for whole-bark preparations, and use without medical supervision is strongly discouraged.

## Scientific Research

The clinical evidence base for Cinchona officinalis as a dietary supplement is limited primarily to preclinical in vitro and in vivo studies, with no recent randomized controlled trials evaluating supplemental doses in human subjects identified in the current literature. Available data include [anti-inflammatory](/ingredients/condition/inflammation) assays using methanol bark extracts showing 17.0–57.3% inhibition relative to diclofenac, albumin denaturation assays demonstrating 18.4–58.5% anti-arthritic inhibition at 75 mg/mL, and DPPH radical scavenging with IC50 values below 25 μg/mL in ethyl acetate fractions—all conducted without reported sample sizes or statistical power. Cytotoxicity studies using quinine-loaded iron oxide nanoparticles on MCF-7 breast cancer cells suggest enhanced anticancer bioavailability compared to free extract, but these lack human translation data. The historical antimalarial use of quinine as an isolated pharmaceutical compound is well-established through decades of clinical application, but this evidence does not directly validate the whole bark or standardized extract as a supplement in modern trial frameworks.

## Historical & Cultural Context

Cinchona officinalis bark was used by indigenous Andean peoples of Peru and Ecuador centuries before European contact, primarily to treat shivering from cold rather than specifically for malaria, though its febrifuge properties were rapidly recognized upon European introduction. Spanish Jesuit missionaries brought the bark to Europe around 1630–1640, where it became known as 'Jesuit's bark' or 'Peruvian bark' and was documented by Cardinal Juan de Lugo as a treatment for the Roman malaria epidemic; Countess Ana de Chinchón, wife of the Viceroy of Peru, is legendarily—though historically debated—credited with popularizing the remedy in Europe. The bark's active ingredient, quinine, was first isolated in 1820 by French chemists Pierre Joseph Pelletier and Joseph Bienaimé Caventou, marking a milestone in pharmaceutical chemistry and enabling standardized dosing that would underpin colonial tropical medicine throughout the 19th century. Cinchona cultivation was strategically transplanted to British India (Nilgiris), Dutch Java, and East Africa during the colonial era to secure supply lines, and quinine remained the primary antimalarial drug until synthetic chloroquine was developed in the 20th century.

## Synergistic Combinations

Quinine has historically been combined with doxycycline or clindamycin in pharmaceutical malaria treatment protocols, where the antibiotic addresses residual parasitemia and reduces the required quinine dose, thereby lowering cinchonism risk—though this is a medical drug combination rather than a supplement stack. In [antioxidant](/ingredients/condition/antioxidant) formulations, cinchona polyphenols may act additively with vitamin C and flavonoid-rich plant extracts, as ascorbic acid regenerates oxidized phenolic radicals and extends their radical-scavenging activity in vitro. Digestive bitter applications of cinchona bark are traditionally paired with gentian root and other bittering agents in aperitif preparations to synergistically stimulate gastric acid secretion and bile flow through shared bitter receptor (TAS2R) activation.

## Frequently Asked Questions

### What is cascarilla bark used for medicinally?

Cascarilla (Cinchona officinalis) bark is primarily used as a source of quinine and related quinoline alkaloids for antimalarial and antipyretic treatment, with traditional applications dating to 17th-century South America and Europe. Preclinical research also demonstrates anti-inflammatory activity (17–57% inhibition vs. diclofenac), antioxidant effects (DPPH IC50 as low as 17.63 μg/mL), and anti-arthritic potential in albumin denaturation assays. Modern supplemental use is limited and unsupported by standardized clinical trials.

### How much quinine is in cinchona bark?

Quinine concentration in Cinchona bark varies significantly by species and plant part: C. ledgeriana contains 5–14% total alkaloids with quinine as the dominant compound, C. succirubra yields 5–7%, and C. calisaya 4–7%. Twigs, stems, and roots can yield 6–15% total alkaloids, while leaves contain less than 1%. Bark used in traditional preparations or pharmaceutical extraction is typically standardized to known alkaloid percentages, with some commercial preparations cited at up to 16% quinine content by bark weight.

### Is cinchona bark safe to take as a supplement?

Cinchona bark is not considered safe for unsupervised self-supplementation due to the narrow therapeutic index of its quinoline alkaloids. At doses sufficient for pharmacological effect, alkaloids can cause cinchonism (tinnitus, nausea, visual disturbances), cardiac arrhythmias via QT prolongation (especially quinidine), hypoglycemia, and hemolysis in G6PD-deficient individuals. It is contraindicated in pregnancy, and no established maximum safe supplemental dose exists for the whole bark or standardized extract in healthy adults.

### What is the difference between quinine and quinidine in cinchona?

Quinine and quinidine are stereoisomers (diastereomers) derived from the same quinoline-quinuclidine scaffold present in Cinchona bark; both possess equivalent febrifugal (fever-reducing) potency but differ in their clinical applications. Quinine is the primary antimalarial alkaloid, acting by inhibiting heme polymerization in Plasmodium parasites, while quinidine is a Class Ia antiarrhythmic pharmaceutical that blocks cardiac sodium and potassium channels to treat atrial fibrillation and ventricular arrhythmias. Quinidine carries greater cardiovascular risk due to its pronounced effect on cardiac conduction, including QT prolongation and risk of torsades de pointes.

### What traditional preparations are made from cinchona bark?

Traditionally, Cinchona bark was prepared as a decoction or cold infusion using 1–3 grams of dried powdered bark per 200 mL of water, consumed once or twice daily for fever and malaria. In 17th-century Europe, it was administered as a powder, dissolved in wine, or as a tincture; modern preparations include ethanol and methanol extracts for laboratory alkaloid isolation, and cinchona features prominently in bitter aperitifs and tonic water (up to 83 mg quinine/L in EU-regulated products). Experimental green nanoparticle synthesis using FeCl3 and bark extract represents the most recent preparation method, developed to improve cellular bioavailability of alkaloids in research settings.

### Does cascarilla bark interact with antimalarial medications like artemisinin or chloroquine?

Cascarilla contains quinine and quinidine, which are themselves antimalarial compounds that work through similar mechanisms as chloroquine, potentially creating overlapping effects or competitive interactions. Concurrent use with prescription antimalarials like artemisinin or mefloquine may increase the risk of adverse effects and should only be done under medical supervision. Healthcare providers should be informed of cascarilla use when antimalarial medications are prescribed to avoid therapeutic duplication or drug interactions.

### What is the most effective form of cascarilla—dried bark, tincture, or standardized extract?

Standardized extracts of cascarilla that are titrated for quinine and quinidine content provide more consistent alkaloid levels than whole dried bark, which varies significantly depending on growing conditions and processing. Tinctures offer improved bioavailability compared to raw bark due to alcohol extraction of the alkaloids, but standardized extracts allow for precise dosing and reliable therapeutic effects. Whole bark preparations are traditional but deliver unpredictable concentrations of active compounds.

### Can cascarilla bark be used safely for treating night sweats or fever in modern supplement protocols?

While cascarilla has historically been used as a febrifuge for fever reduction, its alkaloid content makes it too potent and risky for self-treatment of common night sweats without medical oversight. The quinine and quinidine in cascarilla can cause cinchonism (headaches, ringing ears, visual disturbances) and may worsen certain cardiac conditions, limiting its practical use as a routine fever remedy today. Modern alternative antipyretics with better safety profiles are generally preferred unless prescribed under professional guidance for specific conditions.

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