Last Updated: November 17 2022

An Ayurvedic herb also classified as a phytopharmaceutical (H15; Europe) which appears to be quite anti-inflammatory, helpful against osteoarthritis, and may help cerebral edema. Boswellia serrata appears to have preliminary evidence for anti-inflammatory joint disorders.

Boswellia is most often used for.

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Sources and Composition



Boswellia serrata (of the family Burseraceae) is a herb which has the gum resin extract used for medicinal purposes related to systemic and topical inflammation. In Ayurveda, this herb is known as Salai guggal and patented in India under Sallaki while being patented in Europe under the name of H15.[1] This is one of a few plants in the species of Boswellia (some important ones being Sacra, carterii,[2] papyrifera, neglecta, rivae,[3] frereana,[4] as well as ovalifoliolata[5]) and 25 species in the Boswellia genus in total.[6]

Boswellia serrata also sometimes referred to as Indian frankincense,[7] and in accordance with this name it has sometimes been traditionally burnt at ceremonies (believed to contribute so spiritual exaltation).[8]

The active component of Boswellia serrata is the oleo-gum resin, a plant exudate that is acquired after an incision into the tree. Traditional preparation of Boswellia gum includes a month-long waiting period where the water leaves this gum as it hardens; which results in a final product of 30-60% resin, 5-10% essential (and aromatic) oils (mostly monoterpenes such as E-beta-ocimene and limonene[9]), with the final 30-55% consisting of polysaccharides.[6]

Historical usage of Boswellia seems to be related to inflammatory conditions, with some religious association as well (which may inflate the renown of the herb; see Ganoderma Lucidum as an example of overpromising historical usage related to royalty)

Various other historical uses of Boswellia is its addition to wine to 'benumb the senses' of prisoners sentenced to death (from the Jewish Talmud, although the original source rather than English translation makes mention that it is used to 'confuse or lose the mind'), and to possess tranquilizing effects (Ethiopia).[8]

Historical case studies of Boswellia, as scientifically invalid as they are, suggest that this gum and its incense are tranquilizing anxiolytics



  • The two 'primary' Boswellic acids 11-keto-β-boswellic acid (KBA; 4.48-5.81mg/g) and 3-O-acetyl-11-keto-β-boswellic acid (AKBA; 32.7-44.2mg/g)[10][7]
  • α-Boswellic acid (αBA; 8.68-16.1mg/g) and its isomer β-Boswellic acid (β-BA; 53.5-246.9mg/g), and the acetylated forms of Acetyl-α-Boswellic and Acetyl-β-Boswellic acid (38.4-192.9mg/g) respectively,[10][7] the other four most research Boswellic acids (which round out the 'main six')
  • 9,11-dehydro-α-Boswellic acid and its isomer (9,11-dehydro-β-Boswellic acid) and their respective acetylated forms (Acetyl-9,11-dehydro-α-Boswellic and Acetyl-9,11-dehydro-β-Boswellic acids)[11]
  • Lupeolic acid and Acetyl-Lupeolic Acid[11]
  • Incensole Acetate,[12] known as a diterpenic cembrenoid.[13] Incensole oxide and Isoincensole oxide may also be found
  • A pentacyclic triterpenediol mixture of 3α,24-dihydroxyurs-12-ene and 3α,24-dihydroxyolean-12-ene[14][15]
  • Serratol[16]
  • α-Thujene[6]
  • α and β-Amyrin[17]
  • Tirucall-8,24-dien-21-oic acids[18]
  • Alpha-pinene and octyl acetate[19]

Beyond those non-caloric bioactives, the actual Boswellia gum does contain a polysaccharide content; these may be bioactive, and are most likely not in concentrated extracts (as concentrated extracts such as 5-Loxin and Aflapin are concentrated for the Boswellic acids):

  • BOS 2000, a polysaccharide involved in immunity[20]

Main three bioactives are considered the 11-keto Boswellic acids (KBA and AKBA) with comparably less research into other boswellic acids but one (β-Boswellic acid) possibly playing an importat role. Beyond that the aromatic compound Incensole appears to be important; amounts listed may not be accurate for patents or extracts with modified total Boswellic acid content


Structure and Properties

The structures for the primary six Boswellic Acids are pictured below. The molecular weights are 456.71 (α and β-Boswellic Acids), 498.75 (Acetylated forms), 470.70 for 11-keto-β-boswellic acid (KBA) and 512.74 for 3-O-acetyl-11-keto-β-boswellic acid (AKBA).[7] Many of these Boswellic Acids, especially AKBA, are hydrophobic (fat-soluble) in nature, as is the other non-Boswellic acid compound known as Incensole Acetate.[21]



5-Loxin and Aflapin

In comparison to a standard Boswellia Serrata extract standardized to 3% 3-O-acetyl-11-keto-β-boswellic acid (AKBA), 5-Loxin appears to induce more cumulative anti-inflammatory effects at the same overall weight due to having a higher concentration of AKBA (30%).[22]

Aflapin is a bioavailability enhanced formulation where the AKBA content is reduced to 20%, but it appears to have better overall antiinflammatory effects (relative to both standard Boswellia Serrata and 5-Loxin) due to having more AKBA reach systemic circulation.[23]

Both formulations are created by and owned by Laila Nutraceuticals of India.


Molecular Targets



Boswellia serrata (via AKBA) appears to inhibit NF-kB activation from TNF-α, IL-1β, doxorubicin, LPS, PMA, H2O2, okadaic acid, and cigarette smoke;[24] all of which actiate NF-kB but from different mechanisms.[25] AKBA also appears to inhibit NF-kB activity in all tested cells demonstrating a ubiquitous effect on NF-kB[24] and is the most potent boswellic acid variant at inhibiting NF-kB and is able to fully abolish activity at 50µM.[24]

It appears that the mechanism by which AKBA acts is, at least in regards to TNF-α, interfering with the phosphorylation of IκBα and Akt (both required for TNF-α induced NF-kB activation[26][27]) and appears to act at a stage upstream of p65.[24]

While the exact mechanism of action is not known, the boswellic acids (most potent is AKBA) appear to inhibit NF-kB in response to pretty much all tested activators of NF-kB and in all tested cell lines



Microtulube proteins (seen as a cytoskeleton of a cell) is important for the structural integrity of a cell, and some toxins that induce amnesia (Colchicine) have been shown to interfere with microtubule formation[28] and stabilizing microtubules may be seen as therapeutic in instances of Alzheimer's Disease[29][30] related to Tau proteins, which may be a biomarker of impaired cellular integrity (as they maintain Microtubule protein constitution inhernetly, and become dissociated when structurally modified leading to neurofibrillary tangles).[31]

Tubulin assembly rate appears to be enhanced when β-boswellic acid is incubated at 150-300uM, with the higher concentration being associated with a near doubling of tubule length thought to be secondary to less disassembly (decrease in β-tubulin GTPase activity with concurrent GTP-cap stabilization).[32] The length of microtubule proteins was enhanced 21.4% and 38.5% at those two concentrations,[32] which are relatively high compared to those found in serum after oral ingestion of Boswellia Serrata.

One other study has noted positive influence on microtubule formation (polymerization) in fetal hippocampal cells at 0.15mM and 0.30mM by 25% and 41.6%.[33]

May enhance microtubule formation and strengthen the constitution of cells, but aside from being preliminary (and not demonstrated in vivo yet) a very high concentration is required for this. Practical relevance unknown





In Caco-2 intestinal cells (in vitro assessment of bioavailability) KBA and AKBA appear to have relatively poor absorption but high retention in intestinal cells,[34] a phenomena associated with highly lipophilic drugs.[35] A later study revisiting the Caco-2 cell model but adding Bovine Serum Albumin to the recieving side noted moderate permeability (hypothesizing an absorption rate between 20-70%) and both KBA and AKBA showing better permeability.[36] Incubation with Vermapril (inhibitor of P-Glycoprotein) showed no influence on kinetics.[36]

Absorption, at the level of the intestinal cell, appears to be quite good for Boswellic acids (for the two 11-keto Boswellic acids, this doesn't seem to reflect serum levels)

The serum levels and subsequent tissue deposition of Boswellic acids can be markedly enhanced via by a lecithin delivery form (Phytosome) of Boswellia extract (known as Casperome™,[37] study duplicated in Medline[38]) a technology used with MERIVA® (a bioavailability enhanced form of curcumin) due to formulation of curcumin with phosphatidylcholine (PC).[39] Serum levels of KBA are increased 7-fold and serum levels of β-Boswellic Acid can be increased 3-fold when compared to standard Boswellia Serrata gum capsules with the same amount of Boswellic Acids (more mass overall due to the use of Phytosome technology) and an equal weight supplement with 39% of the initial content of Boswellic acids still outperforms standard Boswellia Serrata.[37]

Interestingly, this study noted that the high degree of variability in serum concentrations was attenuated with the use of this phospholipid-based delivery system; KBA had ranges exceed the actual serum value at most time points following oral administration of standard Boswellia Serrata (ie. 164.39+/-197.40ng/mL) while the use of the Boswellia serrata extract formulated with phospholipids both enhanced absorption while reducing variability (corresponding time point of equal weight supplement was 165.86+/-87.37ng/mL, equal boswellic acid content was 506.33+/-233.98ng/mL).[37]

Lecithin delivery form (Phytosome) of Boswellia extract enhance delivery of Boswellic acids to serum, thought to be mediated at the levels of the intestines. Enhanced intestinal absorption reduces the variability in serum



In response to 1400mg taken thrice daily (4800mg; free living conditions) Boswella Serrata gum resin, 11-keto-β-boswellic acid (KBA) was detected in a very variable range of 6.4-247ng/mL (0.01–0.5μM) between 14 participants, with one nonresponder (no detectable levels) and two respondents between 100-247ng/mL, all others (n=11) in the range of 6.4-64.2ng/mL, and the total oral intake of KBA was 423.6mg (all values steady state serum levels).[7] A case study of oral KBA intake (1800mg Boswellia Extract) noted a Cmax after one hour with detectable serum levels for 8 hours,[1] whereas rat studies that measuring the time-course of serum levels note that while all six boswellic acids are detected within 30 minutes of oral ingestion that peak levels appear to be around 4-5 hours, with fairly steady concentrations between 3 and 6 hours (study terminated at 6 hours)[40] Other standard pharmacokinetic parameters measured in rats following ingestion of 240mg/kg Boswellic Acid are a Tmax of 2.83+/-2.91(KBA), 3.17+/-1.17(AKBA), 5.50+/-2.17(αBA), 6.00+/-1.79(AαBA), 4.50+/-2.35(βBA), 6.33+/-1.51(AβBA) and a half-life of 0.74(KBA), 6.73+/-5.25(AKBA), 5.49+/-0.79(αBA), 5.38+/-3.23(AαBA), 10.12+/-8.29(βBA), 6.05+/-0.37(AβBA).[37]

3-O-acetyl-11-keto-β-boswellic acid (AKBA) was detected at 15.5ng/mL (0.03uM) in one out of 14 tested patients, and not detectable in the others at 1400mg thrice daily oral intake (4800mg) in free living conditions with a total oral intake of 80.4mg AKBA (all values steady state serum levels),[7] the level of detectable AKBA in this study (15.5ng/mL) being comparable to that found in a previous study using 2400mg Boswellia extract in three subjects over 4 weeks.[41] However, another study that paired Boswellia with fatty foods noted that serum levels reached 28.8ng/mL with food and recorded serum levels of 6ng/mL without,[42] and another study noting the average AUC of AKBA being increased by 55% (72.2+/-44.6ng/mL to 112.1+/-57.4ng/mL).[43] Increased absorption of KBA has been noted as well as AKBA when paired with a fatty meal, where the 75% response rate (if KBA was at all detected in serum) was increased to 92% and increased the Cmax and AUC by 31.2% and 37.2% without affecting Tmax or half-life.[43]

The other four Boswellic acids at 1400mg thrice daily oral intake in free living conditions (The basic α and β isomers and their acetylated versions) also highly variable in the range of 0.5ng/mL to 12ug/mL (12,000ng/mL).[7] The overall ranges for these four Boswellic acids were 36.7-4830.1ng/mL (967.2mg; α-Boswellic Acid), 87.0-11948.5ng/mL (2236.8mg; β-Boswellic Acid), 73.4-2985.8ng/mL (73.2mg; Acetyl-α-Boswellic Acid) and 131.4-6131.3ng/mL (228mg; Acetyl-β-Boswellic Acid). All values are steady state serum levels.[7]

All six primary boswellic acids are found in plasma, with the 'main' boswellic acid of 3-O-Acetyl-11-keto-β-boswellic acid sometimes not being detectable; all boswellic acids also exert very high variability in plasma following oral administration in humans (unreliable)

AKBA can be enhanced with fatty food intake, and liposomes can enhance absorption of all Boswellic aids; the high variability of serum concentrations still exists to a degree, however

One study measured serum levels of lesser studied triterpenoids in a case study of a single patient, and noted serum levels of 0.06umol/L (35mg; 9,11-dehydro-α-BA), 0.1umol/L (12mg; 9,11-dehydro-β-BA), 0.47umol/L (162mg; Acetyl-9,11-dehydro-α-BA), 0.29umol/L (101mg; Acetyl-9,11-dehydro-β-BA) with no detectable serum levels of Lupeolic and Acetyl-lupeolic acid (510mg and 226mg) after 10 days of supplementation.[11]

Other boswellic acids may be absorbed; as it was a case study variability cannot be assessed. Lupeolic acids not detected in serum



The 6 primary Boswellic acids have been detected in tissues of rats following oral administration of 240mg/kg Boswellia (86.97mg/kg total Boswellic acids) in the eyes, liver, kidney, and skeletal muscle (brain also recorded, but discussed in the Neurology section).[37]

In the eyes, median values recorded over 6 hours reach concentrations of 5.67(KBA), 25.59(AKBA), 41.82(αBA), 8.04(AαBA), 123.4(βBA), 24.65(AβBA). In skeletal muscle, median values are 47.05(KBA), 79.81(AKBA), 105.67(αBA), 6.72(AαBA), 260.24(βBA), 35.02(AβBA).[37]

In the liver these median values are 868.49(KBA), 687.00(AKBA), 1188.48(αBA), 252.56(AαBA), 1012.29(βBA), 743.65(AβBA) and in kidney tissues they reached 226.7(KBA), 885.2(AKBA), 1486.6(αBA), 151.24(AαBA), 3208.8(βBA), 494.46(AβBA).[37]

All the above values are ng/g concentrations and are subject to high variability; variability is reduced and overall concentrations increased in response to Phytosome delivery.[37]

All six boswellic acids have been found in liver, kidney, retinal, and skeletal muscle tissues as well as the brain and serum



AKBA and KBA (the 11-keto Boswellic acids) appear to have high affinity for serum albumin.[44]



KBA, β-Boswellic Acid, and α-Boswellic Acid appear to be subject to Phase I metabolism in the liver, without being significantly affected by Phase II in vitro.[36] Mono or polyhydroxylated derivates (di- and tri-) appear to be the predominant metabolites of these unacetylated boswellic acids.[36]

Acetylated Boswellic acids (AKBA, Acetyl-β-Boswellic acid, and Acetyl-α-Boswellic Acid) appear to be rather resistant to metabolism in vitro in liver microsomes,[36] implicating the acetyl moiety at position 3 in attenuating metabolism rates of Boswellic Acids.[45]

Hydroxylation occurs to non-acetylated Boswellic acids, whereas Acetylated Boswellic acids appear to be resistant to metabolism


Enzymatic Interactions

Although inhibiting P-Glycoprotein (with Vermapril) does not appear to inhibit the uptake of Boswellic Acids,[36] the two 11-keto Boswellic acids themselves appear to inhibit the P-Glycoprotein inhibitor.[46]





All six primary Boswellic acids appear to be able to reach the brain after oral administration, with levels in the brain of rats given 240mg/kg (aqueous extract) Boswellia Serrata reaching (at 8 hours after ingestion) for 11-keto-β-boswellic acid (2.38mg/kg; 11.6+/-12.6ng/g), 3-O-Acetyl-11-keto-β-boswellic acid (1.91mg/kg; 37.5+/-56.8ng/g), β-boswellic acid (7.03mg/kg; 1066.6+/-781.6ng/g), Acetyl-β-boswellic acid (5.4mg/kg; 163.7+/-248.9ng/g), α-boswellic acid (3.36mg/kg; 485.1+/-363.8ng/g), and Acetyl-α-boswellic acid (1.68mg/kg; 43.0+/-55.7ng/g).[36] This study noted that the average brain levels of β-boswellic acid of 2.33umol/g wet weight fall within the pharmacological range and suspect that this is the active component for neural issues.[36]

Another study has assessed neural tissue concentrations of KBA and AKBA to levels of 99ng/g and 95ng/g (respectively) following oral intake of 240mg/kg Boswellia extract.[40] These higher concentrations were achieved with crushed H15 capsules, which are in the range of 10.6% KBA and 2% AKBA, higher oral doses relative to the previous study.

AKBA may cross the blood brain barrier easier than KBA in vivo when assessing the ratios of serum to neural concentrations, but does not tend to reach overall higher amounts due to the lesser amount in Boswellia extracts.[40]

All main Boswellic Acids show neural permeability, with the same degree of variance seen in serum

When using a phytosome delivery system (enhanced bioavailability), concentrations of Boswellic acids in the brain can be enhanced, relative to the same oral dose of Boswellic acids without enhanced delivery, from undetectable to 62.1ng/g (KBA), 9.63ng/g to 314.91ng/g (AKBA; ), undetectable to 886.64ng/g (βBA), 7.34ng/g to 120.34 (AαBA), 9.63ng/g to 381.86ng/g (αBA), and undetectable to 402.96ng/g (AβBA).[37]

Phytosome delivery results in significantly higher concentrations in brain tissue following oral administration



Incensole Acetate has been found to activate neural TRPV3 receptors (different than Evodia Rutaecarpa; which acts on TRPV1). TRPV3 is a thermoreceptor with a threshold temperature 31–39°C expressed in epithelial cells of the skin and oropharynx[47][48][49] and elicits a warming sensation upon activation. Incensole Acetate activates calcium influx through TRPV3 with an EC50 of 16uM (with 500uM being as effective as 10mM Camphor, another known TRPV3 agonist), with minimal efficacy on TRPV1 and 4 and no influence on TRPV2.[8] Incensole has been investigated whether it possesss affinity for (and subsequently failed to show any appreciable affinity) for Adrenoreceptors (Alpha 1 and 2; Beta 1 and 2), adenosine A3, Dopamine D1 and D2, Histamine H1 and H2, Tachykinin NK1 or NK2, Muscarinic acetylcholine, 5-HT, Benzodiazepine nor Opioid while not interacting with acetylcholinesterase nor the Norephinephrine transporter.[8]

In the hippocampus, mRNA levels of CRF (regulator of corticosteroids) is dose-dependently reduced following injections of Incensole Acetate, and significantly reduced corticosterone levels in a breed of mice (submissive) with higher resting corticosterone levels; no significant effect in wild type mice.[12] The mRNA levels of CRFR1 and both receptors (mineralocorticoid and glucocorticoid receptors) were unaffected.[12] Many modulatory effects on c-Fos activity have been noted in areas pertaining to stress as well.[8]

Incensole Acetate, a bioactive not belonging to the Boswellic acid family, appears to act as a TRPV3 agonist and may have adaptogenic effects by this novel mechanism

β-Boswellic Acid was able to, in vitro with fetal hippocampal neurons at 10, 20, and 30nM over a period of 8 days, was able to enhance length of neurons (58%, 109%, and 158%) and the mean number of neuronal branches (87%, 139%, and 251%).[33]

Some potential enhancement of neuronal branching and growth, unknown relevance in vivo

A methanolic extract of Boswellia socotrana has been found to have potent anti-cholinesterase properties with 22.32% inhibition at 0.05mg/mL and 71.21% inhibition at 0.2mg/mL, whereas another tested species (elongata) inhibited 11.23% and 46.34% respectively.[50] Anti-cholinesterase properties have been detected with boswellic acids previous (in particular, 11-hydroxy-β-Boswellic Acid from Boswellia Carterii[50]) so it is possible that Boswellia Serrata possesses these properties. It is currently unexplored

Theoretically possible for Boswellia Serrata to have acetylcholinesterase inhibiting properties, as it has been noted with the species before; unexplored



A controlled study in mice where 1 hour of Ischmia (deprivation of oxygen) was followed by 24 hours of Reperfusion (resupply of oxygen coupled with oxidative damage) had intravenous Incensole Acetate administered at 1, 10, or 50mg/kg during Reperfusion found that the lesions in control were reduced by 22.3%, 57.8%, and 69.6% respectively.[51] Protection from neurological deficit induced by I/R injury followed a similar dose-dependent trend, and the mechanisms were thought to be secondary to anti-inflammation (with 50mg/kg reducing proinflammatory cytokines by 88% (TNF-α), 77% (IL-1β) and 80% (TGF-β) while suppressing NF-kB activity up to 84% at the highest dose and in a dose-dependent manner).[51] This protective effect was acute in nature, as starting intravenous application of Incensole Acetate 6 hours after reperfusion (rather than immediately) attenuated the reduction in infarct size form 77% to 37%.[51]



Boswellia Serrata gum was assigned the orphan drug status for the reduction of peritumoral edema by the European Medicines Agency (EMA) in 2002, where it goes by (in Europe) the name of H15.[52] A series of case studies in 12 persons with cerebral edema (7 glioblastoma, 2 anaplastic astrocytoma, two low-grade astrocytoma, and one with cerebral metastases from malignant melanoma) either off or on a stable dose of corticosteroids were given 1200mg H15 thrice a day (3600mg total) for 12 weeks was associated with reduced edema in 2/7 tumor bearers but benefitted all patients with edema due to radiotherapy.[52] Out of the 7 patients with tumors, no tumor responded to Boswellia and overall Boswellia was well tolerated.[52] Similar results have supposedly been found in a clinical trial mentioned in some studies,[53] where 30 patients with glioblastoma recieving 1200mg thrice daily Boswellia extract had less peritumoral edema accompanied with a general improvement of well being. The trial (Winking M et al; Boswellic acid as an inhibitor of the perifocal edema in malignant glioma in man. Neurooncology 1996) is not located online.

Appears to have limited but promising clinical effectiveness in reducing neural edema associated with radiotherapy

In a small unblinded study of 4 persons with chronic cluster headaches who also reported disturbed sleep (due to the headaches) given 350-700mg Boswellia Serrata thrice daily (1050-2100mg total) for up to 3 months noted resoluations in nocturnal headaches in all four subjects and an attenuation of overall headache severity and frequency.[54] It should be noted that cluster headaches have edema as a possible sign.[55]

Basically case studies (so not the most statistically sound), but shows promise for cluster headaches



A constituent of Boswellia known as Incensole (Acetate) appears to have anti-depressant effects in the Forced Swim Test in mice when injected with 50mg/kg acutely[8] and is effective at 10mg/kg in submissive mice.[12] Lower doses appear effective over time, with 1-5mg/kg in the submissive mice (10-50% acute dose) having similar effects after 1 week of ingestion.[12]

When 10mg/kg in submissive mice was compared to Paroxetine at 10mg/kg, it was technically not statistically different although underperformed,[12] while in normal mice given 50mg/kg it was less effective than 5mg/kg Diazepam in a Forced Swim Test.[8] Anti-depressant effects of Incensole Acetate may be mediated by TRPV3 receptors, as mice lacking these receptors do not have anti-depressant effects in response to injected Incensole.[8]



A constitient of Boswellia known as Incensole Acetate has failed to significantly influence anxiety at the same dose required to exert anti-depressive effects, 10mg/kg in submissive mice.[12] A reduction in anxiety has been seen at 50mg/kg in otherwise healthy mice as assessed by an elevated plus maze (with comparable effects to Diazepam).[8]

Anxiolytic effects of Incensole Acetate may be mediated by TRPV3 receptors, as mice lacking these receptors do not have anxiolytic effects in response to injected Incensole.[8]



A constitient of Boswellia known as Incensole Acetate has failed to significantly influence locotmotion at the same dose required to exert anti-depressive effects.[12] A reduction in locomotion has been noted in otherwise healthy mice given 50mg/kg Incensole.[8]



One study using Boswellia papyrifera (similar assortment of bioactives, but may not apply to Serrata) as a 300mg/kg ethanolic extract orally thrice a day (900mg/kg total dose) for 4 weeks showed significant reductions in escape latency and travel distance in a water platform finding test; suggesting improved spatial memory formation.[56] These effects were also seen with isolated Boswellic Acids, and 300mg/kg Boswellic acids thrice a day (900mg/kg) was as effective at enhancing spatial memory formation as the active control of Nicotine (as tartrate salt; 1mcg infusion into the brain daily) although 100mg/kg thrice a day (300mg/kg) was also effective.[56]


Cardiovascular Health



8 hours after consumption of 800mg Boswellia Serrata, there appears to be reduced collagen and arachidonic acid-induced blood clotting in otherwise healthy persons with no effect on Thrombin formation;[43] this was attributed to inhibition of cathepsin G,[41] but was deemed to be weak when compared to Naproxen.[43]



Endothelial cells respond to TNF-α (a pro-inflammatory cytokine), and 22% of the genes influenced by TNF-α (n=552) are influenced by Boswellic Acids,[22] particularly those related to proteolysis, cell adhesion, and inflammation.[57] Three metalloproteins (MMP-3, 10, and 11) are potently suppressed in HMECs (endothelial cells) with incubation of Boswellic acids, with more potency being derived from a mixture with a higher concentration of 3-O-Acetyl-11-keto-β-Boswellic Acid (AKBA) where TNF-α induced MMP release was almost abolished.[22] These effects may underlie the protection seen with AKBA in ApoE-/- mice, where 100umol/kg injections of AKBA halved the size of lesions induced by LPS, a proinflammatory molecule[58] and to explain a reduction in TNF-α induced ICAM-1 secretion in vitro (ICAM-1 being an adhesion factor).[59] It should be noted that the direct sequestering of LPS applies to β-Boswellic Acid and not AKBA, and cannot explain these observed results.[58]

The anti-inflammatory effects of AKBA may be cardioprotective by reducing inflammation and atherosclerosis; this has been seen in vivo after injections, but practical significant of oral ingestion is not known (AKBA tends to have low oral absorption)


Fat Mass and Obesity



A component of Boswellia known as Incensole (Acetate) appears to actiate TRPV3, a receptor upon which activation induces the sensation of warmth;[8] this is a mechanism similar to Evodia Rutaecarpa, and the sensation of warmth may create a false positive for fat loss (despite no energy being expended to produce heat, but merely a sensory change).

Warmth from Boswellia Serrata (currently not demonstrated to be an effect) may be a false positive for fat loss due to having

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