Bee venom

Bee Venom (Apitoxin)

Identity, Source, and Common Preparations

Systematic and common names: Bee venom is formally known as apitoxin and is produced by Apis mellifera (the European honeybee), the species studied most extensively in both traditional and scientific contexts. Although Apis mellifera venom has been studied the most extensively, there are several other Apis species, namely Apis cerana and Apis florea, whose venom and/or peptides have also shown promising pharmacological effects and anticancer properties.

Physical characteristics: Bee venom is an odorless and transparent liquid containing a hydrolytic mixture of proteins with acid pH (4.5 to 5.5) that bees often use as a defense tool against predators. One drop of bee venom consists of 88% water and only 0.1 µg of dry venom. In general, the pH of bee venom is 5.2 to 5.5, indicating acidity, and its specific gravity is 1.313.

Source: Bee venom is produced by female worker bees. It is primarily used as a defensive mechanism against threats to the hive, such as predators.

Venom collection: Collection uses an apparatus involving a low voltage electric shock method. The extractor consists of two wooden frames, one inside the other, and pure liquid bee venom is deposited on the underside of a silicone rubber sheet.

Common preparations and dosage forms: Bee venom is administered in several distinct ways in both traditional and clinical settings:

• Live bee sting therapy: Live bee sting therapy involves deliberately introducing bee venom into the body via a live bee's sting.
• Bee venom acupuncture (BVA) / apipuncture: Bee venom is commonly used to alleviate pain, primarily through injections at acupuncture points, such as ST36 (Zusanli). One variation, apipuncture, involves using bee venom to stimulate acupuncture points on the patient's body, merging traditional acupuncture methods with the medicinal benefits of bee venom. The venom is directly administered to specific acupuncture points chosen based on traditional Chinese medicine or other acupuncture-based medical systems.
• Purified and standardized extracts: To purify crude bee venom, the extract is subjected to a stepped-gradient open column. Using this method, the yield of melittin is significantly increased and the allergen proteins are effectively removed. The melittin content of the purified bee venom is determined using HPLC, and the product is then diluted to 0.1 mg/mL using injection water in preparation for pharmacopuncture.
• Topical forms: The types of bee venom treatments used in clinical trials included acupuncture, ointment, and ultrasound gel. Ointments and ultrasound gel, which are externally applied, were used for the treatment of muscle soreness and temporomandibular disorder.
• Sweet bee venom (SBV): Since the mid-2000s, in order to reduce the adverse reactions of bee venom, a method has been in use to remove its components that cause side effects, such as phospholipase A2, and extract and purify only the active ingredient, melittin, thereby creating what is called sweet bee venom (SBV).
• Venom immunotherapy (VIT) extracts: Used for desensitization in allergy management, discussed in the relevant clinical section below.

Traditional and Historical Use

Hymenoptera venom therapy, in particular that involving bee venom (apitoxin), was practiced in ancient Egypt, Greece, and China, and was improved by modern studies of apitherapy during the 19th century.

References to possible medical properties of bee products can be found in Chinese, Korean, Russian, Egyptian, and Greek traditional medicine practices. Apitherapy has been practiced since the times of Hippocrates and Galen.

Hippocrates himself used bee venom for healing purposes, calling it Arcanum, and historical figures such as Charlemagne and Ivan the Terrible resorted to bee stings to find relief from gout. In traditional Chinese medicine, bee venom was employed in acupuncture and other therapeutic techniques.

In some Eastern European countries and China, apipuncture is even combined with traditional acupuncture, creating an integrated approach that unites two age-old wisdoms.

Among beekeepers, an empirical observation has always been known that has fascinated generations: those who work daily with bees and receive regular stings tend to suffer less from rheumatic pain.

The transition from purely empirical use to more formal medical investigation occurred in the 19th century. Modern use of bee venom appears to have originated with Austrian physician Philipp Terč, and his 1888 article "About a Peculiar Connection Between the Bee Stings and Rheumatism," but his claims were never tested in proper clinical trials. More recent alternative medicine practice is attributed to the Hungarian physician Bodog F. Beck who coined the term "bee venom therapy" in 1935, and to beekeeper Charles Mraz (1905–1999) in the latter half of the twentieth century. In 1957, the USSR Ministry of Health sanctioned use of bee venom to treat certain ailments by approval of Nikolay Artemov's "Instruction for Bee Sting Venom Apitherapy."

Precise knowledge of the composition and mode of action of such venom dates back only 50 years. The advent of electrophoresis, chromatography, and gel-filtration, together with pharmacological and biochemical techniques, brought about the identification of a number of components of bee and wasp venoms.

Key Constituents and Active Compounds

Bee venom is a biochemically complex substance. It is known to contain many active components including: (i) peptides like melittin, apamin, mast cell degranulating (MCD) peptide, and adolapin; (ii) enzymes, such as phospholipase A2 (PLA2) and hyaluronidase; and (iii) amino acids and volatile compounds. In addition, bee venom contains many low molecular mass compounds, such as sugars, amino acids, phospholipids, and pheromones.

Melittin

Melittin makes up approximately 40–60% of the total dry weight of bee venom, making it the dominant substance by a wide margin. It is a linear, water-soluble peptide consisting of 26 amino acid residues with a molecular weight of about 2840 Da. It is often described as an "anti-microbial peptide (AMP)."

Pore formation induced by melittin is responsible for its hemolytic, antimicrobial, antifungal, and antitumor activities. Melittin has been shown to cause neural plastic changes along pain-signaling pathways by activation and sensitization of nociceptor cells. The mechanism involves the phosphorylation of mitogen-activated protein kinases (MAPK) as well as the activation of thermal nociceptive channels like TRPV1 (transient receptor potential vanilloid receptor 1), ATP-gated P2X and P2Y purinergic receptors.

At low concentrations, melittin induces mast cell degranulation; at high concentrations, it has anti-inflammatory effects.

Melittin binds directly to p50 and inhibits NF-κB activation in LPS-induced mouse models of Alzheimer's disease and microglial BV-2 cells.

Phospholipase A2 (PLA2)

Phospholipase A2 (PLA2) accounts for around 12–15% of the dry weight of the venom and is the second-most prevalent component in bee venom. Concerning its primary structure, it is composed of a single polypeptide chain consisting of 128 amino acids, characterized by an active site (-CCxxHDxC-), and a calcium-binding loop.

PLA2 is the major allergen in bee venom. Bee venom PLA2 induces a T helper type 2 (Th2) cell-type response and group 2 innate lymphoid cell activation via the enzymatic cleavage of membrane phospholipids and release of interleukin-33.

PLA2 is the enzyme that is the major allergen in bee venom, and PLA2 secreted from bee venom is associated with inflammation and pain.

Apamin

Apamin contributes about 2% of bee venom's dry weight. It is composed of 18 amino acid residues and is stabilized by two disulfide bonds. Apamin's ability to cross the blood-brain barrier has opened up research into treatments for neurodegenerative diseases.

MCD Peptide, Adolapin, and Other Components

Bee venom compounds, including melittin, apamin, secapin, MCD peptide, tertiapin, hyaluronidase, and phospholipase A2, act synergistically, contributing to the overall bioactivity exerted by bee venom, inducing cytolytic, neurotoxic, pro-inflammatory, allergenic, and antimicrobial effects.

MCD peptide blocks arachidonic acid and inhibits prostaglandin synthesis. Adolapin inhibits microsomal cyclooxygenase and also inhibits lipoxygenase and thromboxane.

Mechanisms of Action

Anti-inflammatory Pathways

There are at least four main compounds of bee venom that present anti-inflammatory properties. The anti-inflammatory activity of melittin has been tested against acne vulgaris, neuroinflammation, amyotrophic lateral sclerosis, atherosclerosis, arthritis, and liver inflammation.

The intraperitoneal and oral administration of bee venom and apamin (0.5 and 1 mg/kg) not only showed a decrease in inflammatory cytokines but also decreased paw edema and pain in induced gouty mice. This could be a response to the lower inflammation produced by the suppression of NF-κB and NLRP3 inflammasome.

Bee venom and melittin decreased the expression of chemokines, such as CCL17 and CCL22, and pro-inflammatory cytokines, including IL-1β, IL-6, and IFN-γ, through the blockage of the NF-κB and STAT signaling pathways in an in vitro study using TNF-α/IFN-γ-stimulated human keratinocytes.

Neuroprotective Mechanisms

Bee venom exerts an inhibitory effect in LPS-induced mouse models of Alzheimer's disease, rheumatoid arthritis, Parkinson's disease, and growth of prostate cancer cells by regulating NF-κB activation.

Anticancer Mechanisms

Proposed mechanisms of action include effects on proliferation and growth inhibition, cell cycle alterations, and induction of cell death through several cancer cell death mechanisms, associated with the activation of phospholipase A2 (PLA2), caspases, and matrix metalloproteinases that destroy cancer cells.

Mechanisms of anticancer action include induction of apoptosis, inhibition of cell proliferation, suppression of NF-κB and PI3K/Akt/mTOR pathways, and modulation of immune responses.

In gastric cancer models, melittin has been shown to initiate mitochondrial-dependent apoptosis, characterized by increased generation of ROS, disruption of the mitochondrial membrane potential, and the release of apoptotic factors such as cytochrome c and endonuclease G.

Scientific Evidence by Area of Use

1. Inflammatory Arthritis and Musculoskeletal Pain

This is the area with the most clinical human data for bee venom as a therapeutic agent.

A systematic review of RCTs found twelve randomized controlled trials, including three on Parkinson's disease, four on arthralgia, four on musculoskeletal disorders, and one on polycystic ovary syndrome. The treated conditions included Parkinson's disease, low back pain, temporomandibular disorder, delayed onset muscle soreness, adhesive capsulitis, pelvic inflammatory disease, knee osteoarthritis, and polycystic ovary syndrome.

Clinical studies involving bee venom acupuncture (BVA) on patients with knee osteoarthritis demonstrated the pain-relieving ability of BVA by stimulating aromatase activation in human leukemic cell lines and human osteoblast cells, leading to estrogen production by bone-derived cells, inhibiting the development of osteoarthritis.

The FDA has approved clinical trials on the use of Apitox® for alleviating pain and swelling associated with rheumatoid arthritis, tendonitis, bursitis, and multiple sclerosis.

Evidence strength: Most studies are limited to preclinical models, with scarce clinical trials validating safety, efficacy, dosing, and delivery mechanisms in humans. Large-scale clinical trials of bee venom therapy are needed to verify statistical differences, and a reporting system for adverse events is also required to increase the safety of bee venom therapy.

2. Parkinson's Disease

A pilot randomized controlled trial recruited 43 adults with idiopathic Parkinson's disease divided into three groups: acupuncture, bee venom acupuncture, and control. All subjects had been on stable anti-Parkinsonian drug treatment for at least one month, and they received treatments twice weekly for eight weeks. The results showed significant improvements in the BVA group on the total Unified Parkinson's Disease Rating Scale (UPDRS) and UPDRS part II.

One study revealed that bee venom and apamin could protect against MPTP-induced dopaminergic cell loss by increasing striatal dopamine levels.

Among three RCTs on Parkinson's disease, the treatment frequency for the two studies showing improvement in the UPDRS score was twice a week.

Evidence strength: Despite positive findings of experimental and early clinical studies, there are only a few published data regarding the efficacy of bee venom for Parkinson's disease. Results are considered preliminary and require larger confirmatory trials.

3. Anticancer Activity

Research on the mechanisms of anticancer activity of bee venom in in vitro and animal model studies shows strong anti-cancer potential of both crude bee venom and its main constituent, melittin, by inducing apoptosis and inhibiting the cell cycle without significantly affecting physiological cells.

Previous studies have indicated that bee venom and its major constituent melittin cause a strong toxic effect on different cancer cells, such as liver, lung, bladder, kidney, prostate, breast, and leukemia cells, while a less pronounced effect was observed in normal non-target cells.

Melittin was the most frequently investigated compound, showing anticancer activity in breast, lung, glioblastoma, and ovarian cancer models, from studies retrieved from PubMed, ScienceDirect, and Scopus from 2010 to 2024. A number of studies documented synergistic effects when melittin was mixed with apamin and PLA2.

Diverse drugs were administered in breast cancer research, including crude bee venom, melittin, phospholipase A2, and their complexes. All drugs reduced the number of breast cancer cells in proportion to dose and time. The mechanisms of anticancer effects included cytotoxicity, apoptosis, cell targeting, gene expression regulation, and cell lysis.

Evidence strength: Melittin and honeybee venom's molecular mechanisms of action have not yet been fully analyzed in studies, and as a result, their best uses in the field of oncology have not yet been thoroughly examined. As of the available literature, anticancer evidence is almost entirely limited to in vitro and animal studies, with no completed large-scale human clinical trials confirming efficacy in cancer treatment.

4. Neuroprotection and Alzheimer's Disease

At a concentration of 0.2 mg/kg, bv-sPLA2 exerts greater neuroprotective effects than melittin at a concentration of 1.6 µg/kg for the same treatment period in an LPS-induced mouse model of Alzheimer's disease; however, the Aβ level was more significantly inhibited in bv-sPLA2-treated mice (34.21%) than in those treated with melittin (16.67%).

Bee venom acupuncture has been commonly used for clinical disorders such as Parkinson disease, neuropathic pain, Alzheimer disease, intervertebral disc disease, spinal cord injury, musculoskeletal pain, arthritis, multiple sclerosis, skin disease, and cancer.

Evidence strength: Neuroprotective effects of bee venom in Alzheimer's disease are supported primarily by animal model data. Clinical evidence in humans remains very limited.

5. Antimicrobial and Antiviral Activity

PLA2 has demonstrated antiviral activity against enveloped viruses, including influenza and HIV, by degrading their lipid envelopes. Melittin showed no toxicity in a study in vivo with mice that before treatment with melittin showed resistance to a lethal dose of influenza A virus.

It has also been suggested that bee venom and, particularly, PLA2 may be used as an antiparasitic agent in the treatment against some organisms such as Trypanosoma brucei brucei or Plasmodium falciparum.

Evidence strength: Antimicrobial and antiviral evidence is predominantly in vitro and animal-based. Human clinical data are absent.

6. Skin Conditions

Bee venom has also aroused interest as a cosmetic ingredient due to its protective, antibacterial, and anti-inflammatory effects on the skin. In relation to inflammatory skin diseases, Cutibacterium acnes plays an important role as it induces the activation of TLR2 and TLR4 that produce the liberation of cytokines and chemokines, such as TNF-α, IL-1β, IFN-γ, and IL-8, inducing the inflammation process, with TLRs modulating the activation of NF-κB and MAPK signaling pathways.

Evidence strength: Largely preclinical; some small clinical pilot data exist but no large RCTs have established efficacy for skin conditions.

7. Venom Immunotherapy (VIT) for Allergy — Strongest Clinical Evidence

The most robustly evidence-based clinical use of bee venom is not therapeutic but rather desensitization for patients with life-threatening bee sting allergy.

Venom immunotherapy (VIT) is considered the gold standard treatment aimed at reducing the risk of systemic reactions in individuals with Hymenoptera venom allergy. VIT provides desensitization to the venom to which the patient is sensitive. This treatment protocol is accomplished by gradually increasing venom doses administered subcutaneously. Successfully applying VIT is an effective method for preventing secondary anaphylactic reactions to bee stings.

A retrospective analysis of 1,258 patients with wasp or bee venom allergy, who were treated with 100–200 µg of Hymenoptera venom as a maintenance dose, showed over 95% achieving tolerance to the sting challenge.

A 1990 study with 242 children and adolescents aged 2–16 years found that only 1% of those stung in a follow-up period of 4 years after stopping allergen immunotherapy (AIT) had another anaphylactic reaction, while this occurred in 18% of the untreated control group.

Success rates for desensitization therapy have been reported to be 75% to 85% effective for honeybee immunotherapy when a maintenance dose of 100 micrograms is reached in adults. An increase to a maintenance dose of 150 to 250 micrograms of bee venom has been reported to improve efficacy for those adults not protected by 100 microgram doses.

Evidence strength: Strong. Multiple controlled clinical trials and large retrospective analyses support the efficacy of VIT for bee venom allergy, with consistently high protection rates documented over decades.

Body Systems and Health Areas Associated with Bee Venom

• Musculoskeletal system: Arthritis (rheumatoid and osteoarthritis), low back pain, tendinopathy, adhesive capsulitis, temporomandibular disorders.
• Neurological system: Parkinson's disease, Alzheimer's disease, neuropathic pain, multiple sclerosis (all primarily preclinical or early-stage clinical).
• Immune system: Bee venom allergy desensitization (VIT), immunomodulation.
• Oncology: Breast, lung, liver, bladder, kidney, prostate, ovarian, and leukemia cancer cell lines (primarily in vitro and animal data).
• Integumentary system: Inflammatory skin diseases including acne, atopic dermatitis.
• Antimicrobial / antiviral: Activity against bacteria, enveloped viruses, and parasites (preclinical).

Dosage Forms and Dosages Reported in Studies

Dosing in bee venom research is highly variable and depends on the clinical indication, route of administration, and preparation used.

• Bee venom acupuncture (BVA) — Parkinson's disease RCT: Among three RCTs on Parkinson's disease, the treatment frequency for the two studies showing improvement in UPDRS score was twice a week.
• BVA injection concentration (pharmacopuncture): The melittin content of the purified bee venom was determined using HPLC, and the product was then diluted to 0.1 mg/mL using injection water in preparation for bee venom pharmacopuncture.
• Animal model (gouty arthritis): The intraperitoneal and oral administration of bee venom and apamin at 0.5 and 1 mg/kg showed a decrease in inflammatory cytokines, paw edema, and pain in induced gouty mice.
• Animal model (Alzheimer's, neuroprotection): At a concentration of 0.2 mg/kg, bv-sPLA2 exerted neuroprotective effects, and melittin was tested at a concentration of 1.6 µg/kg in an LPS-induced mouse model of Alzheimer's disease.
• Venom immunotherapy (VIT) — allergy desensitization: Success rates for desensitization therapy have been reported to be 75%–85% effective for honeybee immunotherapy when a maintenance dose of 100 micrograms is reached in adults. An increase to a maintenance dose of 150–250 micrograms of bee venom has been reported to improve efficacy for those adults not protected by 100 microgram doses.
• VIT — high-dose maintenance: In a retrospective analysis of 1,258 patients, those treated with 100–200 µg Hymenoptera venom as a maintenance dose showed over 95% achieving tolerance to the sting challenge.
• Injection site testing (skin test): A suitable testing area such as the flexor surface of the forearm is used at about half the normal dose, or 0.05 mL, slowly injected. A normal response involves a wheal having a diameter of 0.5 to about 1.0 cm and erythematous changes surrounding the injection site. If no systemic reactions occur within 15 to 30 minutes after injection, the test is considered negative.

Note on dosage standardization: Only 27 studies among those reviewed for adverse events specified the capacity of bee venom used. Adverse events associated with bee venom may vary depending on the dosage, method, route of administration, and the country, region, and user. There is currently no universally accepted standard dosing protocol for therapeutic bee venom applications outside of venom immunotherapy.

Safety Considerations and Adverse Events

Anaphylaxis and Severe Allergic Reactions

The most serious adverse events that can occur with bee venom treatment are anaphylaxis and unrecoverable sequelae. Since there is a possibility of anaphylaxis, it is recommended that a person with medical knowledge manage patients undergoing a bee venom procedure.

A systematic review found that the overall incidence rate of anaphylaxis in response to bee venom acupuncture was 0.045% (95% CI 0.028–0.062). In general, the incidence of mild adverse reactions to BVA, such as localized edema, pruritus, and skin rash, was reported to be 28.87%. There were also case reports of two deaths due to anaphylaxis after BVA treatment.

Severe anaphylaxis affects the respiratory and cardiovascular systems. The characteristic symptoms are bronchospasm and shortness of breath, tachycardia, hypotension, sweating, and loss of consciousness. Urinary and fecal incontinence occurs with severe circulatory dysregulation, and the most severe systemic reactions lead to cardiac and respiratory arrest.

Common Adverse Events in Clinical Trials

The most common symptoms caused by bee venom in RCTs were skin reactions at the injection sites, including pruritus, rash, and swelling. Systemic symptoms such as headache, nasopharyngitis, and pain in an extremity were also reported. In a meta-analysis, only itchiness occurred significantly more often in the bee venom group than in the control group (risk ratio = 6.68, 95% confidence intervals: 2.37, 18.84, p < 0.0003, I² = 19%).

In some studies, granulomas or plaques were observed weeks or months after bee venom acupuncture treatment, but in RCTs, the follow-up period is short, so it is less likely to observe these adverse events within the study period.

Risk Factors

Mastocytosis is the most important risk factor for severe sting-induced anaphylaxis. Hereditary α-tryptasemia was recently identified as a genetic predictor of severe reactions. Older age is clearly associated with an increased risk.

Studies have indicated that serious systemic reactions related to stings occur in adults at a rate of 1.2–4.3%, in children at 0.2%, and in beekeepers at 6.5%.

Cross-Reactivity with Honey

Eight allergenic fractions of bee venom have also been identified in honey, which explains frequent adverse reactions after consuming honey in people allergic to venom and sheds new light on the causes of allergic symptoms in some individuals after honey consumption.

Beta-Blockers and ACE Inhibitors

Recent data do not support an aggravation of venom-induced anaphylaxis by intake of β-blockers or angiotensin-converting enzyme (ACE) inhibitors.

Pre-treatment Screening

To reduce the occurrence of serious adverse events in clinical practice, skin tests should be conducted prior to treatment. In a review of relevant RCT studies, there were no studies with a low risk of bias, underscoring the need for improved methodology in this field.

Overall Evidence Quality Assessment

Despite extensive evidence supporting the anti-inflammatory and therapeutic potential of bee venom and its components like melittin, apamin, and PLA2 across diverse disease models, several research gaps remain. Most studies are limited to preclinical models, with scarce clinical trials validating safety, efficacy, dosing, and delivery mechanisms in humans. Furthermore, the mechanisms underlying bee venom's immunomodulatory and antioxidant effects require deeper molecular investigation, especially in chronic and complex diseases.

References

• Bee Venom: Overview of Main Compounds and Bioactivities for Therapeutic Interests — PMC (2019)
• Therapeutic Bioactivity Exerted by the Apis mellifera Bee Venom and Its Major Protein Melittin: A Scoping Review — PMC (2025)
• Bee Venom and Its Sub-Components: Characterization, Pharmacology, and Therapeutics — PMC (2021)
• Melittin—A Natural Peptide from Bee Venom Which Induces Apoptosis in Human Leukaemia Cells — PMC (2020)
• Three Valuable Peptides from Bee and Wasp Venoms for Therapeutic and Biotechnological Use: Melittin, Apamin and Mastoparan — Toxins, MDPI (2015)
• Apitherapy — Wikipedia
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• Bee Venom Soluble Phospholipase A2 Exerts Neuroprotective Effects in a Lipopolysaccharide-Induced Mouse Model of Alzheimer's Disease via Inhibition of Nuclear Factor-Kappa B — PMC (2019)
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