BD-AcAc2
Based on 1 Customer Validation
BD-AcAc2 (R,S-1,3-Butanediol acetoacetate diester) is an orally active, CNS-penetrant antiepileptic agent. BD-AcAc2 inhibits NF-κB, NLRP3 inflammasome, caspase-1/3, pyroptosis, apoptosis, and enhances autophagy. BD-AcAc2 exhibits antioxidant activity by modulating ROS, MDA, SOD, and GSH levels, and alleviates oxidative stress. BD-AcAc2 mitigates chronic colitis, counteracts Dextran Sodium Sulfate (DSS)-induced pathology, protects against central nervous system oxygen toxicity and acute lung injury, and exhibits anti-seizure efficacy. BD-AcAc2 can be used for the research of colitis, sarcopenia, acute lung injury, seizure, and obesity.
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- CAS No.: 58213-75-5
- 화학식: C12H18O6
- 분자량:258.27
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보관:Pure form -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
- 순도&문서
- References
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Help & FAQs
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Biological Activity
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NLRP3 inflammasome |
BD-AcAc2 (4% w/w; p.o.; 24 days) induces nutritional ketosis in healthy rats without altering normal colonic structure[1].
BD-AcAc2 (25% of dietary kcals; dietary; 9 weeks) prevents age-related increases in fat mass in mice[2].
BD-AcAc2 (2.5-10 g/kg; p.o.; single dose) protects mice from central nervous system oxygen toxicity and concomitant acute lung injury in a dose-dependent manner[3].
BD-AcAc2 (4 g/kg; i.g.; single dose) significantly increases blood βHB levels and raises the PTZ seizure threshold in rats[4].
BD-AcAc2 (30% of dietary energy; p.o.; 12 weeks) reduces body weight and adiposity in HFD-induced obese mice[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague Dawley (male, 7 weeks old, 180-200 g, chronic ulcerative colitis induced by 2% DSS for 7 days, followed by 1% DSS for 10 days, then 2% DSS for 7 days)[1]
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Dosage:4% w/w
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Administration:p.o.; ad libitum; 24 days
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Result:Increased plasma β-hydroxybutyrate levels, achieving nutritional ketosis.
Significantly reduced the percentage of body weight loss compared to DSS-only rats.
Significantly decreased the colon weight-to-length ratio compared to DSS-only rats.
Significantly reduced the disease activity index and macroscopic damage index compared to DSS-only rats.
Increased survival rate compared to DSS-only rats.
Significantly lowered the colonic inflammation score compared to DSS-only rats.
Significantly suppressed DSS-induced increases in ROS and MDA levels, and significantly reversed DSS-induced decreases in SOD and reduced GSH levels.
Significantly reduced DSS-induced increases in colon tissue levels of pro-inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-18, and reduced IL-4 levels.
Significantly reversed DSS-induced increases in MPO activity, NF-κB DNA binding activity, caspase-1 activity, and active caspase-3 levels.
Significantly reduced DSS-induced increases in NLRP3 mRNA expression, NLRP3 protein levels, and gasdermin D N-terminal fragment (NGSDMD) levels.
Significantly increased BECN1 levels and decreased p62 levels compared to DSS-only rats, indicating enhanced autophagy.
Significantly increased colon tissue levels of tight junction proteins ZO-1, OCLN, and CLDN5 compared to DSS-only rats.
Significantly reversed DSS-induced changes in gut microbiome composition: reduced relative abundance of Fusobacterium spp., Clostridium spp., and increased relative abundance of Bifidobacterium spp. and Lactobacillus spp.
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Animal Model:Sprague Dawley rats (male, 7 weeks old, 180-200 g)[1]
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Dosage:4% w/w
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Administration:p.o.; 24 days
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Result:Increased plasma β-hydroxybutyrate levels, achieving nutritional ketosis.
Showed normal colonic mucosal architecture with regular rounded mucus-secreting glands and intact goblet cells, matching untreated normal rats.
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Animal Model:C57BL/6J mice (male, 72 weeks of age, naturally aged to 83 weeks)[2]
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Dosage:25% of dietary kcals
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Administration:dietary; ad libitum; 9 weeks
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Result:Showed no within-group change in body weight over time.
Prevented within-group increase in fat mass over time.
Increased expression of 6 skeletal muscle genes and decreased expression of 23 skeletal muscle genes.
Reduced fatty acyl chains in triacylglycerol in skeletal muscle.
Increased levels of 11 skeletal muscle proteins and decreased levels of 33 skeletal muscle proteins compared to controls.
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Animal Model:C57BL/6 mice (male, 20 g)[3]
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Dosage:2.5; 5.0; 10.0 g/kg
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Administration:p.o.; single dose (20 minutes before hyperbaric oxygen exposure)
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Result:Prolonged CNS oxygen toxicity seizure latency in a dose-dependent manner.
Increased mean seizure latency.
Significantly reduced hyperbaric oxygen-induced increases in brain malondialdehyde content.
Substantially alleviated hyperbaric oxygen-induced lung damage including congestion, inflammatory cell infiltration, and structural distortion, with only mild pulmonary vasodilation observed in treated groups.
Showed no effect on lung malondialdehyde content, as hyperbaric oxygen exposure did not affect this parameter.
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Animal Model:Wistar rats (male, 250 g)[4]
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Dosage:4 g/kg
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Administration:i.g.; single dose
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Result:Increased urethane-corrected PTZ seizure threshold.
Raised blood βHB levels.
Confirmed a significant treatment effect on PTZ threshold.
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Animal Model:C57BL/6J mice (male, 5 weeks of age at study start, HFD-induced obesity)[5]
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Dosage:30% of dietary energy
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Administration:p.o.; 12 weeks
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Result:Reduced final body weight.
Reduced final fat mass.
Lowered mean energy intake.
Increased adjusted resting energy expenditure (REE) and total energy expenditure (TEE) significantly compared to pair-fed controls.
Increased adjusted dark cycle REE and TEE compared to both continuous HFD and pair-fed controls.
Elevated circulating β-hydroxybutyrate concentration to 0.51 mM, higher than continuous HFD and pair-fed controls.
Increased mRNA expression of uncoupling protein-1, deiodinase-2, and peroxisome proliferator-activated receptor γ coactivator-1α in interscapular brown adipose tissue (BAT) compared to pair-fed controls.
Increased UCP1 protein expression in BAT compared to pair-fed controls.
Reduced hepatic triglyceride levels.
Lowered fasting serum insulin.
Decreased glucose tolerance test incremental area under the curve (AUCI) and insulin tolerance test AUCI compared to continuous HFD controls, similar to pair-fed controls.
Chemical Information
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CAS No. 58213-75-5
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Appearance Liquid
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분자량 258.27
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화학식 C12H18O6
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SMILES
O=C(CC(C)=O)OCCC(C)OC(CC(C)=O)=O
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Synonyms
R,S-1,3-Butanediol acetoacetate diester
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Pure form -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
순도&문서
References
[1]. Saber S, Alamri MMS, Alfaifi J, et al.. (R,R)-BD-AcAc2 Mitigates Chronic Colitis in Rats: A Promising Multi-Pronged Approach Modulating Inflammasome Activity, Autophagy, and Pyroptosis. Pharmaceuticals (Basel, Switzerland). 2023 Jul 03;16(7):953. [Content Brief]
[2]. Roberts BM, et al. Effects of an exogenous ketone ester using multi-omics in skeletal muscle of aging C57BL/6J male mice. Front Nutr. 2022 Nov 15;9:1041026. [Content Brief]
[3]. Yi H, Yu S, Zhang Y, et al.. Preventive effects of ketone ester BD-AcAc on central nervous system oxygen toxicity and concomitant acute lung injury. Diving and hyperbaric medicine. 2018 Dec 24;48(4):235-240. [Content Brief]
[4]. Viggiano A, Pilla R, Arnold P, et al.. Anticonvulsant properties of an oral ketone ester in a pentylenetetrazole-model of seizure. Brain research. 2015 Aug 27;1618:50-4. [Content Brief]
[5]. Davis RAH, Deemer SE, Bergeron JM, et al.. Dietary R, S-1,3-butanediol diacetoacetate reduces body weight and adiposity in obese mice fed a high-fat diet. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2019 Feb;33(2):2409-2421. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
BD-AcAc2 Related Classifications
HY-159007 Related Classifications
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- BD-AcAc2
- 58213-75-5
- R,S-1,3-Butanediol acetoacetate diester
- Pyroptosis
- NF-κB
- NOD-like Receptor (NLR)
- Caspase
- Apoptosis
- Autophagy
- Reactive Oxygen Species (ROS)
- Oxidative Phosphorylation
- Interleukin Related
- NLRP3 inflammasome
- apoptosis
- gut barrier function
- autophagy
- skeletal muscle regeneration
- pyroptosis
- NFκB
- caspase-1
- caspase-3
- Sprague Dawley rats
- Inhibitor
- inhibitor
- inhibit