+86-28-82633987
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 product of the pentacyclic triterpene acid derived from the oil resin of the bark of the Boswellia serrata tree. As one of the most representative active components in frankincense, 11-KBA has attracted attention for its remarkable anti-inflammatory, antioxidant, and antitumor properties. In recent years, with in-depth research into its molecular mechanisms, 11-KBA has been identified as a novel Nrf2 activator and selective 5-lipoxygenase (5-LOX) inhibitor, demonstrating potential therapeutic value in various disease models, especially in cardiovascular diseases, neurodegenerative diseases, and metabolic disorders. This paper systematically reviews the chemical structure, plant origin, pharmacological activity, mechanism of action, druggability evaluation, and clinical application prospects of 11-KBA, aiming to provide theoretical basis and research directions for further development and application of this natural product.
11-Keto-boslavic acid belongs to the pentacyclic triterpenic acid class of compounds, with a molecular formula of C_30H_46O_4 and a molecular weight of 470.68. Its structural feature is that the β-bostilate backbone contains a ketone group (C=O) at position 11, a structural modification that gives it 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 Ų, and it has 4 hydrogen bond acceptors, indicating certain polarity and binding potential in intermolecular interactions. Toxicological evaluation showed that the LD50 of 11-KBA reached 2000 mg/kg, with no significant hepatotoxicity, cardiotoxicity, or hERG channel inhibition. Ames-induced mutagenic tests were negative, indicating good safety.
11-Ketone Boswellic acid mainly comes from the oleoresin secreted from the bark of the Boswellia serrata tree, commonly known as Indian Frankincense. The Frankincense tree belongs to the Burseraceae family, widely distributed in India and the Middle East. Traditionally, resin secreted after the bark of the Frankincense tree is cut is collected after drying, and used as a traditional medicinal material for anti-inflammation, pain relief, and immune regulation.
Common methods for extracting 11-KBA include solvent extraction, supercritical fluid extraction, and column chromatography separation. Typically, 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 CO_2 extraction technology has gradually been applied to extract active components of frankincense resin due to its environmental friendliness and high efficiency, effectively retaining the bioactive components of 11-KBA.
As a selective 5-lipoxygenase (5-LOX) inhibitor, 11-KBA can block the synthesis of leukotriene and suppress the release of inflammatory mediators, thereby exerting significant anti-inflammatory effects. Numerous in vitro and in vivo studies have shown that 11-KBA effectively inhibits the activation of nuclear factor κB (NF-κB), reduces the expression of tumor necrosis factor α (TNF-α) and other pro-inflammatory cytokines, and alleviates inflammatory responses. Its anti-inflammatory effects have shown good efficacy in models of 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. Studies show that 11-KBA significantly reduces cell death and serum lactate dehydrogenase (LDH) levels in an oxygen and glucose deprivation (OGD)-induced oxidative damage model, demonstrating dose-dependent cardioprotective effects. This characteristic gives it potential application value in the prevention and treatment of ischemia-reperfusion injury and cardiovascular diseases such as myocardial infarction.
11-KBA exhibits antiproliferative and pro-apoptotic effects across various tumor cell lines. Its mechanism involves inhibiting the NF-κB signaling pathway, reducing the expression of pro-tumor factors, and regulating the expression of cyclins and apoptosis-related proteins. Additionally, 11-KBA can inhibit tumor cell invasion and metastasis by regulating redox states and the inflammatory microenvironment. Related in vivo experiments further confirmed its inhibitory effect on tumor growth, providing a theoretical basis for its role as a candidate anti-tumor drug.
11-KBA also shows certain regulatory effects on hyperglycemia and related metabolic diseases. Its targets involve various metabolic regulatory proteins such as EHMT2, UBP2, PAI1, AMPK, SGLT2, GCK, APP, BACE1, CES1, and PTPN1, suggesting that it may coordinately regulate blood glucose metabolism, insulin sensitivity, and lipid metabolism through multiple targets, and has potential application value for antidiabetic and related complications.
The multiple pharmacological effects of 11-KBA are attributed to its regulation of key molecular targets:
5-Lipidoxidase (5-LOX) inhibition: 11-KBA competitively inhibits 5-LOX activity, blocks leukotriene synthesis, reduces the release of inflammatory mediators, and alleviates inflammatory responses.
Nrf2/HO-1 signaling pathway activation: 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 the NF-κB signaling pathway: By inhibiting IκBα degradation, it blocks NF-κB nuclear translocation, lowers the expression of pro-inflammatory factors such as TNF-α and IL-1β, and exerts anti-inflammatory and antitumor effects.
Regulatory metabolic targets: 11-KBA affects AMPK activity and promotes energy metabolism balance; Inhibiting SGLT2 reduces renal glucose reabsorption; Regulates proteins such as EHMT2 and PTPN1, improving insulin signaling and glyco-lipid metabolism.
The synergistic effect of these mechanisms enables 11-KBA to demonstrate broad therapeutic potential across various pathological states.
The physicochemical properties of 11-KBA show high lipid solubility (LogP=6.0), which helps with cell membrane penetration but may limit its water solubility and oral bioavailability. Its TPSA is 74.6, and its hydrogen bond receptor count is 4, meeting certain drug compatibility standards. Toxicological data indicate that 11-KBA has a high safety profile, with an LD50 of 2000 mg/kg, no significant hepatotoxicity, cardiotoxicity, or mutagenicity, and does not inhibit hERG channels, reducing the risk of arrhythmias.
The lower permeability of the blood-brain barrier suggests that its direct role in central nervous system diseases may be limited, but this also reduces potential CN toxicity. Pharmacokinetic research is still in its early stages. Current data indicate that 11-KBA is widely distributed in the body, has stable metabolism, and is mainly excreted via hepatic metabolic pathways. In the future, further systematic evaluation of its absorption, distribution, metabolism, and excretion (ADME) characteristics is needed to optimize administration methods and formulation design.
Based on the multi-target and multi-mechanism effects of 11-KBA, its clinical application prospects are broad in anti-inflammation, antioxidant, cardiovascular protection, and antitumor fields. Especially in adjunctive therapy for rheumatoid arthritis, inflammatory bowel disease, ischemic heart disease, and certain tumors, 11-KBA has the potential to become a novel natural drug.
Additionally, 11-KBA regulates multiple metabolic-related targets, demonstrating its potential for application in diabetes and metabolic syndrome. In the future, modern drug design technologies can be combined to develop derivatives or combination formulations to improve bioavailability and targeting, expanding clinical indications.
However, current clinical research on 11-KBA remains limited, urgently requiring systematic clinical pharmacology and safety evaluations to clarify its optimal dosage and administration regimen. At the same time, in-depth analysis of its mechanism of action and pharmacokinetic characteristics will provide a solid foundation for its clinical translation.
As an important active component of pentacyclic triterpenic acid in the frankincense tree, 11-keto frankincense acid demonstrates broad medicinal value due to its unique chemical structure and diverse pharmacological activities. By selectively inhibiting 5-LOX, activating the Nrf2/HO-1 antioxidant pathway, and suppressing NF-κB inflammatory signaling, it achieves multiple biological effects including anti-inflammatory, antioxidant, and antitumor effects. Good safety and druggability lay the foundation for its clinical development. In the future, as pharmacological mechanisms are further revealed and clinical research advances, 11-KBA is expected to become a novel natural drug for treating inflammatory diseases, cardiovascular diseases, and metabolic disorders, providing new strategies and options for the prevention and treatment of related diseases.
Shenshuai
Wenjing
Hedandan
