Supplements

Boswellia

Updated · 34 sources · Editorial policy

Boswellia is the gum resin of Boswellia serrata, a tree native to India, the Middle East and North Africa, also known as Indian frankincense, and the extracts made from it. The resin has been used for centuries in Ayurvedic medicine (LiverTox). Today it is sold as a dietary supplement for joint pain, mostly osteoarthritis, and is also promoted for colitis and asthma. Its main active compounds are thought to be boswellic acids, especially acetyl-11-keto-β-boswellic acid (AKBA).

The most important fact is that the clinical evidence is mostly small, short and product-specific. Several meta-analyses of knee osteoarthritis trials report less pain with boswellia than with placebo. But many of the trials were small, used different proprietary extracts and were often funded by the companies that sell them. The anti-inflammatory mechanism usually cited, blocking the enzyme 5-lipoxygenase, has been shown in the lab but not clearly in people.

This page summarizes what clinical trials, meta-analyses and NIH resources report. It is for education only and is not medical advice.

Property Detail
Type Botanical extract; dietary supplement
Source Gum resin of Boswellia serrata (Indian frankincense)
Main active compounds Boswellic acids (pentacyclic triterpene acids), including AKBA, KBA and β-boswellic acid
Standardized extracts studied 5-Loxin (≥30% AKBA); Aflapin (≥20% AKBA plus a non-acidic resin fraction)
Route Oral
Doses in trials 100–250 mg/day of AKBA-enriched extracts in osteoarthritis; 900–4,200 mg/day of resin or extract in asthma, colitis and brain-edema trials
Half-life KBA ≈6 h after a single 333 mg dose; AKBA ≈6.8 h in one formulation study
Key mechanism (lab data) Inhibits 5-lipoxygenase and microsomal prostaglandin E synthase-1 in cell and enzyme assays
US status Sold as a dietary supplement; not an approved drug
WADA status Not listed on the 2026 Prohibited List

What it is

Boswellic acids

Boswellia resin contains a family of triterpene acids called boswellic acids. Pharmacokinetic studies measure six major ones (Riva et al., Phytomedicine 2016):

Boswellic acid Abbreviation Note
3-O-acetyl-11-keto-β-boswellic acid AKBA Most potent 5-lipoxygenase inhibitor in lab assays; C₃₂H₄₈O₅, 512.7 g/mol (PubChem)
11-keto-β-boswellic acid KBA Second “keto” acid; used with AKBA as a quality marker
β-boswellic acid βBA Weaker on 5-lipoxygenase but reaches far higher blood levels
α-boswellic acid, and the acetylated forms of α- and β-boswellic acid αBA, AαBA, AβBA αBA and AαBA were detectable in plasma only when taken with a high-fat meal in one study (Sterk et al., Planta Med 2004)

KBA and AKBA are the marker compounds in the European Pharmacopoeia monograph for Indian frankincense, and many supplements advertise their KBA or AKBA content (Abdel-Tawab et al., Clin Pharmacokinet 2011).

Standardized extracts

Commercial products differ widely. A 2021 analysis found “striking differences” in boswellic acid content between frankincense products. The authors linked this to different Boswellia species and different extraction methods (Börner et al., Pharmaceuticals 2021; funded by a pharmacy company whose CEO was a co-author). Two Indian extracts from the same developer are among the most studied:

Extract Composition reported by its developer Developer and funding
5-Loxin B. serrata extract standardized to at least 30% AKBA Laila Impex; the 2008 trial was funded by Laila Impex and co-authored by its employees (Sengupta et al., Arthritis Res Ther 2008)
Aflapin AKBA-enriched extract combined with a non-volatile oil fraction of the resin; at least 20% AKBA Laila; the 2010 comparison trial was “supported by Laila Nutraceuticals,” and 3 authors listed Laila Impex R&D as their affiliation (Sengupta et al., Int J Med Sci 2010)

Other products tested in trials include H15 and Boswelan (extracts used in German Crohn’s disease trials) and lecithin or micellar formulations made to improve absorption.

Mechanism: what lab studies show

The classic explanation comes from rat cells. In rat neutrophils, boswellic acids blocked the formation of leukotriene B4, an inflammatory signal made by the enzyme 5-lipoxygenase (5-LOX). AKBA was the strongest, with an IC50 (concentration that gives half-maximal inhibition) of 1.5 µM. In isolated human platelets, boswellic acids up to 400 µM did not inhibit cyclooxygenase (the target of NSAIDs) or 12-lipoxygenase (Safayhi et al., J Pharmacol Exp Ther 1992).

Later work questioned whether this happens in people:

  • Albumin blocks the effect. In isolated human neutrophils, the keto boswellic acids inhibited 5-LOX at IC50 2.8–8.8 µM. In human whole blood they did not. Adding albumin abolished the effect, apparently because over 95% of the acids bind to it (Siemoneit et al., Eur J Pharmacol 2009).
  • No effect in volunteers. In the same study, a single 800 mg dose of frankincense extract did not lower plasma leukotriene B4 in healthy volunteers.
  • Other targets. Boswellic acids inhibit microsomal prostaglandin E synthase-1 (mPGES-1), which makes the inflammatory prostaglandin PGE2, at IC50 3–10 µM. β-boswellic acid lowered PGE2 in human whole blood in the lab and reduced inflammation in rats and mice (Siemoneit et al., Br J Pharmacol 2011).

A 2011 review concluded that the 5-LOX explanation is “questionable.” Plasma levels of AKBA and KBA after oral doses are far below the levels active in lab assays. β-boswellic acid reaches about 100-fold higher plasma levels, which makes mPGES-1 and the protease cathepsin G more plausible targets (Abdel-Tawab et al., Clin Pharmacokinet 2011). All of this is cell, enzyme and animal data. No study has shown which mechanism, if any, explains the effects reported in clinical trials.

Pharmacokinetics

Boswellic acids, especially AKBA, are poorly absorbed:

  • Gut permeability. In human intestinal (Caco-2) cell models, AKBA crossed poorly and KBA moderately; most of both stayed in the cell layer (Krüger et al., Eur J Pharm Sci 2009).
  • Metabolism. In human and rat liver microsomes, KBA was extensively oxidized, while AKBA was not, and AKBA was not converted to KBA (Krüger et al., Drug Metab Dispos 2008).
  • Food. Taking 786 mg of extract with a high-fat meal raised the peak levels and total exposure of βBA, KBA and AKBA “several-fold” compared with fasting in healthy men (Sterk et al., Planta Med 2004).
Study Product and dose Result
Sharma et al., Phytomedicine 2004, 12 healthy men 333 mg B. serrata extract, single dose KBA peak at 4.5 h; elimination half-life 5.97 h
Kulkarni et al., Drug Metab Pers Ther 2021, 10 healthy volunteers 333 mg solid-lipid particle formulation AKBA peak 8.04 ng/mL (≈0.016 µM) at 1.5 h, half-life 6.8 h; KBA peak 23.83 ng/mL, half-life 2.45 h
Schmiech et al., Phytomedicine 2024, 20 healthy volunteers, crossover 800 mg micellar vs standard extract Micellar form raised relative bioavailability of boswellic and lupeolic acids to 1,720–4,291%, highest for AKBA
Riva et al., Phytomedicine 2016, 12 volunteers, crossover 500 mg lecithin formulation vs standard extract Faster and higher absorption of the major boswellic acids except KBA (the first four authors were affiliated with Indena S.p.A.)

Better absorption has not been shown to mean a better effect. In the 2024 micellar study, higher blood levels did not improve anti-inflammatory activity in blood samples tested outside the body (ex vivo), and the standard extract did slightly better on one cytokine (Schmiech et al., Phytomedicine 2024).

Regulatory status

  • United States. Boswellia is sold as a dietary supplement. A 2021 review noted that frankincense preparations are marketed as nutraceuticals but have not been approved as drugs (Börner et al., Pharmaceuticals 2021).
  • European Union. In 2002 the European Medicines Agency gave B. serrata extract orphan-drug designation for peritumoral brain edema (swelling around brain tumors) (Abdel-Tawab et al., Clin Pharmacokinet 2011). A designation is not an approval.
  • Sport. Boswellia and boswellic acids do not appear on the WADA 2026 Prohibited List.

What the research shows

Knee osteoarthritis: meta-analyses

Osteoarthritis is the use with the most trials. Pooled results generally favor boswellia over placebo for short-term pain and function, but the reviews disagree on how much to trust them.

Review Trials and participants Main finding
Ernst, BMJ 2008 (all conditions) 7 RCTs All reported benefit; 3 of good quality; evidence “encouraging but not compelling”
Cameron & Chrubasik, Cochrane 2014 5 studies of 3 boswellia extracts 100 mg/day enriched extract for 90 days (2 studies, 85 people): pain −17 points on a 0–100 scale (95% CI 8–26) vs placebo; function −8 points (95% CI 2–14)
Liu et al., BJSM 2018 (20 supplements) 69 studies in total Boswellia among 7 supplements with large short-term pain effects (effect size over 0.80); no supplement had clinically important long-term effects; evidence quality very low to high
Bannuru et al., Semin Arthritis Rheum 2018 (with curcumin) 11 RCTs, n = 1,009 Boswellia better than placebo for pain and function; study quality low overall; no trials against approved NSAIDs
Yu et al., BMC Complement Med Ther 2020 7 RCTs, n = 545 VAS pain WMD −8.33 (95% CI −11.19 to −5.46); WOMAC pain WMD −14.22 (95% CI −22.34 to −6.09); heterogeneity very high (I² 94–99%)
Dalmonte et al., Phytother Res 2024 13 studies; 850 (WOMAC) and 1,185 (VAS) patients Overall effect not significant because of high heterogeneity (p = 0.087 WOMAC; p = 0.40 VAS); significant benefit only in the placebo-controlled subgroup
Dubey et al., Explore 2024 9 RCTs, n = 712 VAS MD −10.71; Aflapin subgroup −16.09 vs −4.68 for other extracts. All three authors were employees of an Indian supplement company
Zhang et al., Nutrients 2025 (network meta-analysis, 7 supplements) 39 RCTs, n = 4,599 Boswellia vs placebo: WOMAC pain MD 10.58 (95% CI 6.45–14.78), VAS pain MD 17.26 (95% CI 8.06–26.52); ranked most likely best for pain and stiffness

In the Cochrane review, the 95% confidence interval for pain included a reduction of 15 points, which the authors treated as clinically important. They still concluded only that boswellia extracts “show trends of benefits that warrant further investigation” (Cameron & Chrubasik, Cochrane 2014).

For other joint supplements, see glucosamine and chondroitin, MSM, collagen peptides and turmeric. In the BJSM meta-analysis, glucosamine, chondroitin and MSM had statistically significant but small effects of unclear clinical importance (Liu et al., BJSM 2018).

Knee osteoarthritis: trial quality

Several issues limit how far these results can be trusted:

  • Small and short. Most trials enrolled fewer than 100 people (Bannuru et al., 2018). Yu et al. rated trial quality “generally medium to low” (Yu et al., 2020). Ernst found small samples and incomplete reporting to be the most common flaws (Ernst, BMJ 2008). No supplement in the BJSM review showed clinically important effects beyond the short term (Liu et al., 2018).
  • Industry funding. The key 5-Loxin and Aflapin trials were funded by the products’ developer and co-authored by its staff. Their abstracts describe the products as “safe for human consumption” and report benefit within 7 days.
  • Different products. Pooled analyses combine extracts with very different compositions, which helps explain the very high heterogeneity.
  • Independent trials are fewer and less positive. The independent Australian ATLAS trial tested a combination of boswellia 250 mg, pine bark 100 mg, MSM 1,500 mg, curcumin 500 mg and piperine 5 mg daily in 84 adults. After 12 weeks, pain fell by about 20 mm in both groups (20.1 vs 20.3 mm on a 0–100 VAS), with no difference from placebo (Yuan et al., Osteoarthritis Cartilage 2026).

The two Laila trials most often cited:

Trial Design and n Arms (daily) Duration Reported result Funding
Sengupta et al., 2008 Double-blind RCT, single center, 75 randomized, 70 completed 5-Loxin 100 mg or 250 mg, or placebo 90 days Both doses improved pain and function vs placebo; 250 mg significant by day 7; lower MMP-3 (a cartilage-degrading enzyme) in joint fluid Laila Impex; 3 authors were company employees
Sengupta et al., 2010 Double-blind RCT, 60 randomized (20 per arm), 57 completed 5-Loxin 100 mg, Aflapin 100 mg or placebo 90 days Both improved pain and function; Aflapin significant by day 7 Laila Nutraceuticals

Inflammatory bowel disease

The IBD evidence comes from a few small trials with mixed results:

Trial Condition and design Dose Result
Gupta et al., Eur J Med Res 1997 Ulcerative colitis; small comparison with sulfasalazine 350 mg gum resin three times daily, 6 weeks Remission 82% vs 75% with sulfasalazine
Gerhardt et al., Z Gastroenterol 2001 Active Crohn’s disease; double-blind non-inferiority trial vs mesalazine, 102 randomized H15 extract CDAI (disease activity score) fell by 90 vs 53 points; non-inferior to mesalazine, not significantly better
Madisch et al., Int J Colorectal Dis 2007 Collagenous colitis; double-blind RCT vs placebo, 31 randomized 400 mg three times daily, 6 weeks Remission 63.6% vs 26.7% per protocol (p = 0.04), but 43.8% vs 26.7% by intention to treat (p = 0.25); no effect on histology
Holtmeier et al., Inflamm Bowel Dis 2011 Crohn’s disease in remission; double-blind RCT vs placebo, 82 randomized Boswelan 2,400 mg/day (6 × 400 mg capsules), 52 weeks Stopped early; remission kept in 59.9% vs 55.3% on placebo (P = 0.85)

The largest and longest placebo-controlled trial, in Crohn’s maintenance, was negative. The positive results come from small trials, active-control designs or per-protocol analyses. Boswellia has no established role in IBD.

Asthma

One 6-week, double-blind trial randomized 40 patients to 300 mg gum resin three times daily and 40 to lactose placebo. It reported improvement in 70% vs 27%, judged from a mix of symptoms, lung function and blood counts (Gupta et al., Eur J Med Res 1998). The groups differed at baseline in age range and sex ratio. Ernst’s 2008 review included this as its only asthma trial and noted that the two groups also differed in asthma severity (Ernst, BMJ 2008). Evidence for asthma is very limited.

Brain edema after radiotherapy

In a pilot double-blind RCT, 44 patients receiving brain radiotherapy took B. serrata 4,200 mg/day or placebo. Edema volume on MRI fell by over 75% in 60% of the boswellia group vs 26% of the placebo group (P = .023). Dexamethasone doses did not differ, and quality of life and cognition were unchanged (Kirste et al., Cancer 2011). The authors called for larger studies.

Side effects and risks

General tolerability

Trials generally report few side effects:

  • Osteoarthritis. The Cochrane review found no serious adverse events. In one study, adverse events were less common with enriched extract than with placebo (18/48 vs 30/48; RR 0.60, 95% CI 0.39–0.92) (Cameron & Chrubasik, Cochrane 2014). Across supplements, safety did not differ from placebo (Liu et al., BJSM 2018).
  • Long-term use. In the 52-week Crohn’s trial (2,400 mg/day), there were no safety disadvantages compared with placebo (Holtmeier et al., 2011).
  • High dose. At 4,200 mg/day, 6 patients reported minor stomach or bowel discomfort; there were no severe adverse events (Kirste et al., 2011).
  • Skin. Allergic contact dermatitis has been reported from a cream containing B. serrata extract (Acebo et al., Contact Dermatitis 2004).

Most trials were small and lasted a few months, so rare or long-term harms cannot be ruled out. We found no safety data for pregnancy or breastfeeding in the sources reviewed.

Liver

LiverTox (NIH) states that B. serrata extracts have not been linked to rises in liver enzymes (aminotransferases) during treatment or to cases of clinically apparent liver injury (LiverTox: Boswellia Serrata). Many joint products combine boswellia with turmeric, which has its own liver-safety profile (see turmeric).

Interactions

No controlled human drug-interaction studies were found. Lab studies suggest some possible interactions:

  • Cytochrome P450 enzymes. Resin extracts of four Boswellia species, including B. serrata, were potent non-selective inhibitors of CYP1A2, 2C8, 2C9, 2C19, 2D6 and 3A4 in vitro. Boswellic acids were not the main inhibiting compounds (Frank & Unger, J Chromatogr A 2006).
  • Drug transporters. In cell assays, KBA and AKBA modulated OATP1B3 and MRP2, two transporters that move many drugs. The authors said “therapeutic relevant interactions with other anionic drugs may be expected” (Krüger et al., 2009).

Whether these effects happen at the low blood levels reached in people is unknown.

Key takeaways

  • A resin extract with variable content. Boswellia supplements contain boswellic acids such as AKBA, but products vary widely, and trial results apply to the specific extract tested.
  • Modest short-term osteoarthritis benefit, low-certainty evidence. Meta-analyses favor boswellia over placebo for knee pain over weeks to a few months. The trials are small, heterogeneous and often funded by manufacturers, and an independent 12-week trial of a boswellia combination found no benefit.
  • Mechanism unproven in humans. 5-lipoxygenase inhibition is clear in lab assays but blocked by albumin in whole blood and not seen in volunteers. Other targets such as mPGES-1 are also lab findings.
  • Poor absorption. AKBA reaches low nanogram-per-milliliter levels in blood. Fat-rich meals and lecithin or micellar formulations raise levels, but this has not been shown to improve effects.
  • IBD and asthma are not established uses. Small early trials were positive, but the longest placebo-controlled Crohn’s trial was negative and asthma rests on one 1998 study.
  • Generally well tolerated. Trials report mainly mild stomach upset, and LiverTox lists no liver injury cases. Drug interactions are possible on lab data but have not been studied in people.

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