Product name: 11-Keto-beta-boswellic acid
Synonym name: 11-Keto-β-boswellic acid; 3-Hydroxy-11-oxo-12-ursen-24-oic acid
Catalogue No.: BP0018
Cas No.: 17019-92-0
Formula: C30H46O4
Mol Weight: 470.694
Botanical Source: Boswellia carteri and Boswellia serrata (Indian olibanum)
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Can be supplied from milligrams to grams.
For Reference Standard and R&D, Not for Human Use Directly.
Inquire for bulk scale.
Description:
11-Keto-beta-boswellic acid, a novel Nrf2 activator, and a selective 5-lipoxygenase (5-LOX) inhibitor; it exerts dose dependent cardioprotective effect manifested by dose-dependent reduction in serum lactate dehydrogenase; and it can increase the Nrf2 and HO-1 expression, which provides protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. 11-Keto-beta-boswellic acid possesses significant anti-inflammatory, and anti-tumoral activities.
References:
Phytochemistry. 2013 Dec;96:330-6.
Biotransformation of 11-keto-β-boswellic acid by Cunninghamella blakesleana.
11-Keto-beta-boswellic acid (KBA), as one of the active constituents in the gum resin of Boswellia serrata, possesses significant biological activities including anti-inflammatory activity. However, its extensive metabolism and low polarity has limited the systemic availability of 11-Keto-beta-boswellic acid. The present research was aimed to obtain and explore the various possible derivatives of 11-Keto-beta-boswellic acidthrough biotransformation by Cunninghamella blakesleana AS 3.970.
METHODS AND RESULTS:
A total of ten transformed compounds were isolated and purified, and their chemical structures were characterized as 7β-hydroxy-11-keto-β-boswellic acid; 7β, 15α-dihydroxy-11-keto-β-boswellic acid ; 7β, 16β-dihydroxy-11-keto-β-boswellic acid; 7β, 16α-dihydroxy-11-keto-β-boswellic acid; 7β, 22β-dihydroxy-11-keto-β-boswellic acid; 7β, 21β-dihydroxy-11-keto-β-boswellic acid; 7β, 20β-dihydroxy-11-keto-β-boswellic acid; 7β, 30-dihydroxy-11-keto-β-boswellic acid; 3α, 7β-dihydroxy-11-oxours-12-ene-24, 30-dioic acid and 3α, 7β-dihydroxy-30-(2-hydroxypropanoyloxy)-11-oxours-12-en-24-oic acid by various spectroscopic methods. The biotransformation processes include hydroxylation, oxidation and esterification. Primary structure-activity relationships (SAR) of inhibitory effects on NO production in RAW 264.7 macrophage cells are discussed.
Eur J Med Chem. 2015 Jul 15;100:98-105.
11-Keto-boswellic acid derived amides and monodesmosidic saponins induce apoptosis in breast and cervical cancers cells.
Beta-boswellic acids are considered the main bioactive components of frankincense. Their potential to act as cytotoxic agents, as well as that of their derivatives remained unexploited so far.
METHODS AND RESULTS:
In this study we were able to prepare derivatives of 11-keto-β-boswellic acid (KBA) that showed lower IC50 values as determined by a sulphorhodamine B (SRB) assay using several different human tumour cell lines. Monodesmosidic saponins of KBA are as cytotoxic as 3-acetyl-KBA. The presence of a free hydroxyl group at position C-3 seems to lower cytotoxicity while the presence of an amide function at C-24 improves cytotoxicity. The most active compound of this series gave IC50 values as low as 4.5 μM.
CONCLUSIONS:
Cell death proceeded mainly via apoptosis.
Mol Neurobiol. 2015 Dec;52(3):1430-1439.
Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia-Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism.
Oxidative stress is well known to play a pivotal role in cerebral ischemia-reperfusion injury. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. 11-Keto-beta-boswellic acid(KBA) is a triterpenoid compound from extracts of Boswellia serrata. The aim of the present study was to determine whether KBA, a novel Nrf2 activator, can protect against cerebral ischemic injury.
METHODS AND RESULTS:
Middle cerebral artery occlusion (MCAO) was operated on male Sprague-Dawley rats. KBA (25 mg/kg) applied 1 h after reperfusion significantly reduced infarct volumes and apoptotic cells as well as increased neurologic scores at 48 h after reperfusion. Meanwhile, posttreatment with KBA significantly decreased malondialdehyde (MDA) levels, restored the superoxide dismutase (SOD) activity, and increased the protein Nrf2 and HO-1 expression in brain tissues. In primary cultured astrocytes, KBA increased the Nrf2 and HO-1 expression, which provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. But knockdown of Nrf2 or HO-1 attenuated the protective effect of KBA.
CONCLUSIONS:
In conclusion, these findings provide evidence that the neuroprotection of KBA against oxidative stress-induced ischemic injury involves the Nrf2/HO-1 pathway.
HPLC of 11-Keto-beta-boswellic acid
HNMR of 11-Keto-beta-boswellic acid
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
74.6000
6.0000
5.0000
Low
95.0000
No
No
No
No
No
No
11 Keto beta boswellic acid (11-KBA) is a natural pentacyclic triterpenoid acid derived from the bark oil resin of Boswellia serrata trees. As one of the most representative active ingredients in frankincense, 11-KBA has attracted much attention due to its significant anti-inflammatory, antioxidant, and anti-tumor activities. In recent years, with in-depth research on its molecular mechanism, 11-KBA has been discovered as a novel Nrf2 activator and selective 5-lipoxygenase (5-LOX) inhibitor, demonstrating potential therapeutic value in various disease models, particularly in cardiovascular disease, neurodegenerative disease, and metabolic disease. This article provides a systematic review of the chemical structure, plant origin, pharmacological activity, mechanism of action, pharmacological evaluation, and clinical application prospects of 11-KBA, aiming to provide theoretical basis and research direction for the further development and application of this natural product.
11 keto frankincense acid belongs to pentacyclic triterpenoid acid compounds, with a molecular formula of C30H46O4 and a molecular weight of 470.68. Its structural feature is the presence of a ketone group (C=O) at position 11 on the β - frankincense skeleton, which endows it with unique biological activity. The LogP value of 11-KBA is about 6.0, indicating high lipid solubility, which helps it penetrate cell membranes but may also limit its water solubility and bioavailability. Its polar surface area (TPSA) is 74.6 Å ² and the number of hydrogen bond acceptors is 4, indicating its polarity and binding potential in intermolecular interactions. Toxicological evaluation shows that the LD50 of 11-KBA is as high as 2000 mg/kg, and there is no significant hepatotoxicity, cardiotoxicity, or hERG channel inhibition. The Ames mutagenicity test is negative, indicating good safety.
11 keto frankincense mainly comes from the oil resin secreted by the bark of Boswellia serrata, commonly known as Indian frankincense. The frankincense tree is a plant of the Burseraceae family, widely distributed in India and the Middle East. Traditionally, the resin secreted by frankincense bark after being cut is collected after drying and used as a traditional medicinal herb for anti-inflammatory, analgesic, and immune regulation purposes.
The common methods for extracting 11-KBA include solvent extraction, supercritical fluid extraction, and column chromatography separation. Usually, the dried frankincense resin is first extracted with ethanol or methanol to obtain a crude extract, which is then purified by silica gel column chromatography or high-performance liquid chromatography (HPLC) to obtain high-purity 11-KBA. In recent years, supercritical CO2 extraction technology has gradually been applied to the extraction of active ingredients from frankincense resin due to its environmental friendliness and high efficiency, which can effectively retain the bioactive components of 11-KBA.
As a selective 5-lipoxygenase (5-LOX) inhibitor, 11-KBA can block the synthesis of leukotrienes, inhibit the release of inflammatory mediators, and thus exert significant anti-inflammatory effects. Numerous in vitro and in vivo studies have shown that 11-KBA can effectively inhibit the activation of nuclear factor kappa B (NF - κ B), reduce the expression of tumor necrosis factor alpha (TNF - α) and other pro-inflammatory cytokines, and alleviate inflammatory responses. Its anti-inflammatory effect has shown good therapeutic effects in disease models such as rheumatoid arthritis, inflammatory bowel disease, and asthma.
11-KBA is a novel Nrf2 activator that can induce Nrf2 nuclear translocation, promote the expression of downstream antioxidant enzymes such as heme oxygenase-1 (HO-1), and enhance the cell's defense against oxidative stress. Research has shown that 11-KBA significantly reduces cell death and serum lactate dehydrogenase (LDH) levels in an oxidative damage model induced by oxygen and glucose deprivation (OGD), exhibiting dose-dependent cardioprotective effects. This characteristic makes it potentially valuable for the prevention and treatment of cardiovascular diseases such as ischemia-reperfusion injury and myocardial infarction.
11-KBA exhibits anti proliferative and pro apoptotic effects in various tumor cell lines. The mechanism involves inhibiting the NF - κ B signaling pathway, reducing the expression of tumor promoting factors, and regulating the expression of cell cycle proteins and apoptosis related proteins. In addition, 11-KBA can also inhibit the invasion and metastasis of tumor cells by regulating the redox state and inflammatory microenvironment. Further in vivo experiments have confirmed its inhibitory effect on tumor growth, providing a theoretical basis for its use as a candidate anti-tumor drug.
11-KBA also exhibits a certain regulatory effect on hyperglycemia and related metabolic diseases. Its target involves multiple metabolic regulation proteins such as EHMT2, UBP2, PAI1, AMPK, SGLT2, GCK, APP, BACE1, CES1 and PTPN1, suggesting that it may regulate blood glucose metabolism, insulin sensitivity and lipid metabolism through multi target coordination, and has potential application value in anti diabetes and its complications.
The multiple pharmacological effects of 11-KBA are attributed to its regulation of key molecular targets:
5-Lipoxygenase (5-LOX) inhibition 11-KBA competitively inhibits 5-LOX activity, blocks leukotriene synthesis, reduces the release of inflammatory mediators, and alleviates inflammatory responses.
Activation of Nrf2/HO-1 signaling pathway 11-KBA promotes the transfer of Nrf2 from the cytoplasm to the nucleus, binds to antioxidant response elements (ARE), upregulates the expression of HO-1 and other antioxidant enzymes, enhances cellular antioxidant capacity, and reduces oxidative stress damage.
Inhibition of NF - κ B signaling pathway By inhibiting the degradation of I κ B α, preventing NF - κ B nuclear translocation, and reducing the expression of pro-inflammatory factors such as TNF - α and IL-1 β, it exerts anti-inflammatory and anti-tumor effects.
Regulating metabolic related targets 11-KBA affects AMPK activity and promotes energy metabolism balance; Inhibiting SGLT2 reduces renal glucose reabsorption; Regulating proteins such as EHMT2 and PTPN1 to improve insulin signaling and glucose and lipid metabolism.
The synergistic effect of these mechanisms enables 11-KBA to exhibit broad therapeutic potential in various pathological states.
The physicochemical properties of 11-KBA indicate its high lipid solubility (LogP=6.0), which facilitates membrane penetration but may limit its water solubility and oral bioavailability. Its TPSA is 74.6 and the number of hydrogen bond receptors is 4, which meets certain drug compatibility standards. Toxicological data shows that 11-KBA has high safety, with an LD50 of 2000 mg/kg, no significant hepatotoxicity, cardiotoxicity, or mutagenicity, and does not inhibit hERG channels, reducing the risk of arrhythmia.
The low permeability of the blood-brain barrier suggests that its direct role in central nervous system diseases may be limited, but this also reduces potential central neurotoxicity. Pharmacokinetic studies are still in the preliminary stage, and existing data indicate that 11-KBA is widely distributed in the body, metabolically stable, and excreted mainly through the hepatic metabolic pathway. Further systematic evaluation of its absorption, distribution, metabolism, and excretion (ADME) characteristics is needed in the future to optimize administration methods and dosage form design.
Based on the multi-target and multi mechanism effects of 11-KBA, its clinical application prospects in anti-inflammatory, antioxidant, cardiovascular protection, and anti-tumor fields are broad. Especially in the adjuvant treatment of rheumatoid arthritis, inflammatory bowel disease, ischemic heart disease, and certain tumors, 11-KBA has the potential to become a new natural medicine.
In addition, 11 KBA regulates a variety of metabolic targets, showing its potential application in diabetes and metabolic syndrome. In the future, modern drug design technology can be combined to develop its derivatives or composite formulations, improve bioavailability and targeting, and expand its clinical indications.
However, current clinical research on 11-KBA is still relatively limited, and there is an urgent need for systematic clinical pharmacology and safety evaluation to clarify its optimal dosage and administration regimen. Meanwhile, in-depth analysis of its mechanism of action and pharmacokinetic characteristics will provide a solid foundation for its clinical translation.
11 keto frankincense acid, as an important active component of pentacyclic triterpenoid acids in frankincense trees, has demonstrated broad medicinal value due to its unique chemical structure and diverse pharmacological activities. It achieves multiple biological effects such as anti-inflammatory, antioxidant, and anti-tumor by selectively inhibiting 5-LOX, activating the Nrf2/HO-1 antioxidant pathway, and inhibiting NF - κ B inflammatory signaling. Good safety and drug properties have laid the foundation for its clinical development. In the future, with the deepening of pharmacological mechanisms and the advancement of clinical research, 11-KBA is expected to become a new natural medicine for the treatment of inflammatory diseases, cardiovascular diseases, and metabolic disorders, providing new strategies and choices for the prevention and treatment of related diseases.
