CAS 67416-61-9|3-O-Acetyl-11-keto-beta-boswellic acid

Introduction：Basic information about CAS 67416-61-9|3-O-Acetyl-11-keto-beta-boswellic acid, including its chemical name, molecular formula, synonyms, physicochemical properties, and safety information, etc.

Table of Contents

1. Names
2. 3-O-Acetyl-11-keto-beta-boswellic acid BiologicalActivity
3. Chemical & Physical Properties
4. Safety Information
5. Synonyms

Common Name	3-O-Acetyl-11-keto-beta-boswellic acid
CAS Number	67416-61-9	Molecular Weight	512.721
Density	1.1±0.1 g/cm3	Boiling Point	600.3±55.0 °C at 760 mmHg
Molecular Formula	C₃₂H₄₈O₅	Melting Point	/
MSDS	ChineseUSA	Flash Point	184.4±25.0 °C

Names

Name	Acetyl-11-keto-b-boswellic acid
Synonym	More Synonyms

3-O-Acetyl-11-keto-beta-boswellic acid BiologicalActivity

Description	Acetyl-11-Keto-β-Boswellic Acid (AKBA) is an active triterpenoid compound from the extract of Boswellia serrate; a novel Nrf2 activator.IC50 value:Target: Nrf2 activatorin vitro: AKBA significantly reduced infarct volumes and apoptotic cells, and also increased neurologic scores by elevating the Nrf2 and HO-1 expression in brain tissues in middle cerebral artery occlusion (MCAO) rats at 48 hours post reperfusion. In primary cultured neurons, AKBA increased the Nrf2 and HO-1 expression, which provided protection against OGD-induced oxidative insult. Additionally, AKBA treatment increased Nrf2 binding activity to antioxidant-response elements (ARE) [1]. AKBA significantly inhibited human colon adenocarcinoma growth, showing arrest of the cell cycle in G1-phase and induction of apoptosis[3]. AKBA triggered significant lipolysis in 3T3-L1 adipocytes as shown by reduced neutral lipids in cytosol and increased free fatty acids in culture medium. Increased lipolysis by AKBA was accompanied by up-regulation of lipolytic enzymes, adipocyte triglyceride lipase (ATGL) and hormone sensitive lipase (HSL), and a decreased expression of lipid droplet stability regulator perilipin. In addition, AKBA treatment reduced phenotypic markers of mature adipocyte aP2, adiponectin and glut-4 in mature adipocytes [5].in vivo: AKBA significantly prevented the formation of intestinal adenomatous polyps without toxicity to mice. AKBA's activity both in the prevention of small intestinal and colonic polyps was more potently than aspirin. Histopathologic examination revealed that AKBA's effect, that is the reduction of polyp size and degree of dysplasia, was more prominent in larger sized polyps, especially those originating in colon [2]. AKBA administration in mice effectively delayed the growth of HT-29 xenografts without signs of toxicity. The activity of AKBA was more potent than that of aspirin [3]. AKBA exhibited anti-cancer activity in vitro and in vivo. With oral application in mice, AKBA significantly inhibited SGC-7901 and MKN-45 xenografts without toxicity [4].
Related Catalog	Signaling Pathways >>Metabolic Enzyme/Protease >>HIF/HIF Prolyl-HydroxylaseResearch Areas >>CancerNatural Products >>Terpenoids and Glycosides

Description

Acetyl-11-Keto-β-Boswellic Acid (AKBA) is an active triterpenoid compound from the extract of Boswellia serrate; a novel Nrf2 activator.IC50 value:Target: Nrf2 activatorin vitro: AKBA significantly reduced infarct volumes and apoptotic cells, and also increased neurologic scores by elevating the Nrf2 and HO-1 expression in brain tissues in middle cerebral artery occlusion (MCAO) rats at 48 hours post reperfusion. In primary cultured neurons, AKBA increased the Nrf2 and HO-1 expression, which provided protection against OGD-induced oxidative insult. Additionally, AKBA treatment increased Nrf2 binding activity to antioxidant-response elements (ARE) [1]. AKBA significantly inhibited human colon adenocarcinoma growth, showing arrest of the cell cycle in G1-phase and induction of apoptosis[3]. AKBA triggered significant lipolysis in 3T3-L1 adipocytes as shown by reduced neutral lipids in cytosol and increased free fatty acids in culture medium. Increased lipolysis by AKBA was accompanied by up-regulation of lipolytic enzymes, adipocyte triglyceride lipase (ATGL) and hormone sensitive lipase (HSL), and a decreased expression of lipid droplet stability regulator perilipin. In addition, AKBA treatment reduced phenotypic markers of mature adipocyte aP2, adiponectin and glut-4 in mature adipocytes [5].in vivo: AKBA significantly prevented the formation of intestinal adenomatous polyps without toxicity to mice. AKBA's activity both in the prevention of small intestinal and colonic polyps was more potently than aspirin. Histopathologic examination revealed that AKBA's effect, that is the reduction of polyp size and degree of dysplasia, was more prominent in larger sized polyps, especially those originating in colon [2]. AKBA administration in mice effectively delayed the growth of HT-29 xenografts without signs of toxicity. The activity of AKBA was more potent than that of aspirin [3]. AKBA exhibited anti-cancer activity in vitro and in vivo. With oral application in mice, AKBA significantly inhibited SGC-7901 and MKN-45 xenografts without toxicity [4].

Related Catalog

Signaling Pathways >>Metabolic Enzyme/Protease >>HIF/HIF Prolyl-HydroxylaseResearch Areas >>CancerNatural Products >>Terpenoids and Glycosides

Chemical & Physical Properties

Density	1.1±0.1 g/cm3
Boiling Point	600.3±55.0 °C at 760 mmHg
Molecular Formula	C₃₂H₄₈O₅
Molecular Weight	512.721
Flash Point	184.4±25.0 °C
Exact Mass	512.350159
PSA	80.67000
LogP	8.00
Vapour Pressure	0.0±3.7 mmHg at 25°C
Index of Refraction	1.549
InChIKey	HMMGKOVEOFBCAU-BCDBGHSCSA-N
SMILES	CC(=O)OC1CCC2(C)C(CCC3(C)C2C(=O)C=C2C4C(C)C(C)CCC4(C)CCC23C)C1(C)C(=O)O
Storage condition	−20°C

Safety Information

Risk Phrases	R36/37/38
Safety Phrases	26
RIDADR	NONH for all modes of transport

Synonyms

3-O-Acetyl-11-keto-β-boswellic acid

Urs-12-en-24-oic acid, 3-(acetyloxy)-11-oxo-, (3α)-

(3α)-3-Acetoxy-11-oxours-12-en-24-oic acid

(3α)-3-(acetyloxy)-11-oxours-12-en-24-oic acid

3-Acetyl-11-keto-β-boswellic Acid

AKBA

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