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Boswellic acid

Alias: alpha-Boswellic acid; 471-66-9; CHEMBL395428; a-Boswellic acid; (3R,4R,4aR,6aR,6bS,8aR,12aR,14aR,14bR)-3-hydroxy-4,6a,6b,8a,11,11,14b-heptamethyl-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicene-4-carboxylic acid; (4R)-3alpha-Hydroxyolean-12-en-24-oic acid; -Boswellic acid; Boswellic acid, alpha;
Cat No.:V13043 Purity: ≥98%
alpha-Boswellic acid (α-Boswellic acid) is a pentacyclic triterpenoid found in frankincense and has anticonvulsant (antiepileptic/antiseizure) and anti-cancer effect.
Boswellic acid
Boswellic acid Chemical Structure CAS No.: 471-66-9
Product category: New1
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
5mg
10mg
Other Sizes
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description
alpha-Boswellic acid (α-Boswellic acid) is a pentacyclic triterpenoid found in frankincense and has anticonvulsant (antiepileptic/antiseizure) and anti-cancer effect. α-boswellic acid can prevent and reduce Alzheimer's disease (AD) markers in animals and may be utilized in Alzheimer's disease (AD) research.
Biological Activity I Assay Protocols (From Reference)
Targets
Natural product; pentacyclic triterpenoid; PI3K/AKT
ln Vitro
In this study, researchers investigated the effects of α-boswellic acid (ABA) as one of the major component of Boswellia serrata resin on primary fetal human astrocytes under a stress paradigm as a possible model for AD through study on Reelin cascade. For this aim, we used streptozotocin (STZ), in which from an outlook generates Alzheimer's hallmarks in astrocytes, and assayed Reelin expression, Tau and Akt phosphorylation as well as reactive oxygen species (ROS) generation and apoptosis in the presences of ABA. Our results indicated that while STZ (100 µM) down-regulated the expression of Reelin, ABA (25 µM) up-regulated its expression (p < 0.01) for 24 h. ABA efficiently reduced hyperphosphorylated Tau (Ser404) in STZ-treated astrocytes (p < 0.01). Furthermore, STZ-induced apoptosis by increasing cleaved caspase three (p < 0.01) and ROS generation (p < 0.01), a further pathological hallmark of Tauopathy. On the other hand, ABA decreased ROS generation and promoted proliferation of astrocytes through elevating Survivin expression (p < 0.01). These results showed that ABA could be considered as a potent therapeutic agent for prevention and decreasing the progression of Alzheimer's hallmarks in astrocytes; however, more in vivo studies would be needed[3].
ln Vivo
Boswellic acids, triterpenoids derived from the genus Boswellia (Burseraceae), are known for their anti-inflammatory and anti-tumor efficacy. Atopic dermatitis is a chronic, non-infectious inflammatory skin disease. However, the effects of α-boswellic acid on atopic dermatitis have not been studied. Therefore, in this study we examined the expression level of pro-inflammatory cytokines, histopathological analysis, and physiological data from BALB/c mice with atopic-like dermatitis induced by 2,4-dinitrochlorobenzene and TNF-α/IFN-γ-stimulated HaCaT cells to better understand the agent's anti-atopic dermatitis efficacy. First, we found that α-boswellic reduced the epidermal thickening, mast cell numbers, and dermal infiltration of 2,4-dinitrochlorobenzene-induced atopic-like dermatitis in BALB/c mice. Furthermore, we also found that α-boswellic acid can restore transepidermal water loss and skin reddening in mice. In human keratinocytes inflamed by TNF-α/IFN-γ, α-boswellic acid inhibited MAP kinase activation and showed a reduction in NF-κB nuclear translocation. Finally, α-boswellic acid can reduce the expression level of cytokines (IL-1β, IL-6, and IL-8) following the stimulation of TNF-α/IFN-γ in HaCaT cells. Taken together, our study suggests that α-boswellic acids are a potential component for the development of anti-atopic dermatitis drugs[1].
The results showed that α-BA reduced injuries associated with the administration of ethanol, gastric juice acidity and the formation of MDA and increased CAT activity and SOD activity and the level of NO and PGE-2 in a dose-depended manner. The expression of both Nrf2 and HO-1 was significantly increased in the group treated with 200 mg/kg α-BA, which suggested that activation of the Nrf2/HO-1 pathway might be critical in α-BA's prevention of gastric ulcers. Conclusions: These findings demonstrate that α-BA decreases oxidative stress and that the Nrf2/HO-1 pathway might play a role in the gastroprotective action of α-BA in ethanol-induced gastric injury in rats.[2]
Cell Assay
MTT Assay[1]
The cell suspension (1 × 105 cells/mL) was cultured in 24-well plates for 24 h. Cells were pretreated with or without α-boswellic acid (1–50 μM) for 1 h, then MTT solution was added and incubated for 4 h. Finally, 200 μL of DMSO was added to each well, and 180 μL was pipetted into 96 wells for absorbance measurement. Absorbance was measured at 550 nm using Tecan’s Sunrise absorbance microplate reader.
Animal Protocol
First, the effect of α-boswellic acid on AD was assessed on DNBC-induced mice. DNBC-induced AD was developed according to a previously reported method. The dorsal hairs of the mice were briefly shaved and then 100 μL and 20 μL of 1% DNCB in ethanol were applied to sensitive dorsal and ear skin for 7 days. Then, from Day 8 to Day 15, 0.5% DNCB solution was re-challenged every three days. The schematic diagram of the animal experiment is shown in Figure 6. Mice were randomly divided into 5 groups, including the normal control group, AD model group (DNCB solution sensitization challenge), α-boswellic acid group (3 and 10 mg/kg), and positive control group dexamethasone (0.5 mg/kg). α-Boswellic acid or dexamethasone was injected intraperitoneally every 3 days from Day 5 to Day 15. On Day 15 before sacrifice, the lesions on the back skin of the mice were photographed, including the erythema, edema, crusting, and exfoliation. The dorsal skin was isolated, the skin tissue port was fixed in 4% paraformaldehyde for histological analysis, and the remaining skin tissue was immediately frozen in liquid nitrogen and then stored at −80 °C for subsequent studies.[1]
The gastroprotection of α-BA was assessed with ethanol-induced gastric lesions model, by histopathological assessment and measuring gastric juice acidity (pH), gastric wall mucus (GWM), prostaglandins E2 (PGE-2), membrane lipids peroxidation (MDA), superoxide dismutase (SOD) activity, catalase (CAT) activity and amount of nitric oxide (NO). The gastroprotective effects of α-BA through the nuclear factor erythroid-2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) anti-oxidative pathway were presented and measured by immunohistochemistry and Western blot.[2]
References

[1]. Evaluation of the Anti-Atopic Dermatitis Effects of α-Boswellic Acid on Tnf-α/Ifn-γ-Stimulated HaCat Cells and DNCB-Induced BALB/c Mice. Int J Mol Sci. 2022 Aug 30;23(17):9863.

[2]. Alpha-boswellic acid protects against ethanol-induced gastric injury in rats: involvement of nuclear factor erythroid-2-related factor 2/heme oxygenase-1 pathway. J Pharm Pharmacol. 2016 Apr;68(4):514-22.

[3]. The Effects of Alpha Boswellic Acid on Reelin Expression and Tau Phosphorylation in Human Astrocytes. Neuromolecular Med. 2017 Mar;19(1):136-146.

Additional Infomation
Alpha-Boswellic acid is a triterpenoid.
alpha-Boswellic acid has been reported in Boswellia sacra, Cyclocarya paliurus, and other organisms with data available.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C30H48O3
Molecular Weight
456.7003
Exact Mass
456.36
Elemental Analysis
C, 78.90; H, 10.59; O, 10.51
CAS #
471-66-9
PubChem CID
637234
Appearance
White to off-white solid powder
Density
1.1±0.1 g/cm3
Boiling Point
552.7±50.0 °C at 760 mmHg
Flash Point
302.1±26.6 °C
Vapour Pressure
0.0±3.4 mmHg at 25°C
Index of Refraction
1.557
Source
Boswellia sacra, Cyclocarya paliurus, etc.
LogP
9.43
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
3
Rotatable Bond Count
1
Heavy Atom Count
33
Complexity
889
Defined Atom Stereocenter Count
9
SMILES
C[C@@]12CC[C@@]3(C(=CC[C@H]4[C@]3(CC[C@@H]5[C@@]4(CC[C@H]([C@]5(C)C(=O)O)O)C)C)[C@@H]1CC(CC2)(C)C)C
InChi Key
BZXULBWGROURAF-IKNLXHIFSA-N
InChi Code
InChI=1S/C30H48O3/c1-25(2)14-15-26(3)16-17-28(5)19(20(26)18-25)8-9-21-27(4)12-11-23(31)30(7,24(32)33)22(27)10-13-29(21,28)6/h8,20-23,31H,9-18H2,1-7H3,(H,32,33)/t20-,21+,22+,23+,26+,27+,28+,29+,30+/m0/s1
Chemical Name
(3R,4R,4aR,6aR,6bS,8aR,12aR,14aR,14bR)-3-hydroxy-4,6a,6b,8a,11,11,14b-heptamethyl-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicene-4-carboxylic acid
Synonyms
alpha-Boswellic acid; 471-66-9; CHEMBL395428; a-Boswellic acid; (3R,4R,4aR,6aR,6bS,8aR,12aR,14aR,14bR)-3-hydroxy-4,6a,6b,8a,11,11,14b-heptamethyl-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicene-4-carboxylic acid; (4R)-3alpha-Hydroxyolean-12-en-24-oic acid; -Boswellic acid; Boswellic acid, alpha;
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO : ~25 mg/mL (~54.74 mM)
Solubility (In Vivo)
Solubility in Formulation 1: 2.5 mg/mL (5.47 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: 2.5 mg/mL (5.47 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (5.47 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.1896 mL 10.9481 mL 21.8962 mL
5 mM 0.4379 mL 2.1896 mL 4.3792 mL
10 mM 0.2190 mL 1.0948 mL 2.1896 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
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Biological Data
  • Effects of α-boswellic acid on TEWL, the stratum corneum hydration, and erythema of atopic dermatitis in DNCB-induced mice. Mice were treated with intraperitoneal injection with boswellic acid. (A) TEWL; (B) stratum corneum hydration; and (C) erythema. Values represent the mean ± SEM from three independent experiments. * p < 0.05 and ** p < 0.01 vs. the DNCB-only-treated group; # p < 0.05 and ## p < 0.01 vs. the untreated group. AD, atopic dermatitis; DNCB, 2,4-dinitrochlorobenzene; TEWL, transepidermal water loss.[1].Evaluation of the Anti-Atopic Dermatitis Effects of α-Boswellic Acid on Tnf-α/Ifn-γ-Stimulated HaCat Cells and DNCB-Induced BALB/c Mice. Int J Mol Sci. 2022 Aug 30;23(17):9863.
  • (A–E) Effects of α-boswellic acid on the TNF-α/IFN-γ-induced proinflammatory cytokines and chemokine mRNA expressions in HaCaT cells. (F–H) Effects of α-boswellic acid on involucrin, filaggrin, and loricrin mRNA expressions in TNF-α/IFN-γ-induced HaCaT cells. HaCaT cells were pretreated with different concentrations of α-boswellic acid—1, 3, and 10 μM—for 20 min, and then the cells were treated with TNF-α/IFN-γ for 6 h. Total RNA was isolated and the mRNA expression level of IL-1β, IL-6, IL-8, MDC, TARC, involucrin, filaggrin, and loricrin were determined using qPCR. Values represent the mean ± SEM from three or four independent experiments. ## p < 0.01 compared with the no-treatment condition; * p < 0.05 and ** p < 0.01 compared with the only TNF-α/IFN-γ treatment condition.[1].Evaluation of the Anti-Atopic Dermatitis Effects of α-Boswellic Acid on Tnf-α/Ifn-γ-Stimulated HaCat Cells and DNCB-Induced BALB/c Mice. Int J Mol Sci. 2022 Aug 30;23(17):9863.
  • (A–C) Effects of α-boswellic acid on the MAP kinases signaling pathway in TNF-α/IFN-γ-induced HaCaT cells. HaCaT cells were pretreated with different concentrations of α-boswellic acid (1, 3, and 10 μM) for 20 min, and then the cells were treated with TNF-α/IFN-γ for 30 min. Western blots were analyzed quantitatively. Values represent the mean ± SEM from the three independent experiments. ## p < 0.01 compared with the no-treatment condition; * p < 0.05 and ** p < 0.01 compared with the only TNF-α/IFN-γ treatment condition.[1].Evaluation of the Anti-Atopic Dermatitis Effects of α-Boswellic Acid on Tnf-α/Ifn-γ-Stimulated HaCat Cells and DNCB-Induced BALB/c Mice. Int J Mol Sci. 2022 Aug 30;23(17):9863.
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