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Hebei Nengqian Chemical Import and Export Co., LTD

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3-ACETYL

CAS NO.67416-61-9

  • FOB Price: USD: 45.00-65.00 /Kilogram Get Latest Price
  • Min.Order: 5 Kilogram
  • Payment Terms: L/C,D/A,D/P,T/T
  • Available Specifications:

    medical grade(1-50)Kilogrammedical grade(50-500)Kilogram

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Product Details

Keywords

  • 11-keto-b-boswellic acid acetate
  • BOSWELLIC ACID, ACETYL KETO
  • 3-Acetyl-11-keto-b-boswellicacid

Quick Details

  • ProName: 3-ACETYL 67416-61-9
  • CasNo: 67416-61-9
  • Molecular Formula: C32H48O5
  • Appearance: Yellow Crystalline Powder
  • Application: Cytosine (C) is one of the four main b...
  • DeliveryTime: 5-7 woking day
  • PackAge: Brown vial or HDPE plastic bottle
  • Port: Qingdao port, Tianjin port
  • ProductionCapacity: 3000 Kilogram/Month
  • Purity: >99%
  • Storage: Cool Dry Place
  • Transportation: Bag or Drum
  • LimitNum: 5 Kilogram
  • packing: According to your request

Superiority

OEM Supply Superior Quality 99% Cytosine CAS 71-30-7

Basic Information:
 

Cytosine (C) is one of the four main bases found in DNA and RNA, along with adenine, guanine, and thymine (uracil in RNA).

Cytosine reagent is used in a wide variety of research applications, as an enzyme-substrate or precursor of effector molecules such as cytosine sugars.

Product Name: Cytosine
Synonyms: 4-AMINO-2(1H)-PYRIMIDINONE;4-AMINO-2(1)-PYRIMIDONE;4-AMINO-2-PYRIMIDINOL;4-AMINO-2-OXO-1,2-DIHYDROPYRIMIDINE;4-AMINO-2-HYDROXYPYRIMIDINE;2-Oxy-4-amino pyrimidine;AURORA KA-682;CYTOSINE
CAS: 71-30-7
MF: C4H5N3O
MW: 111.1

 

Details

Molecular Formula C32H48O5
Molar Mass 512.73
Density 1.13±0.1 g/cm3(Predicted)
Melting Point 271℃
Boling Point 600.3±55.0 °C(Predicted)
Specific Rotation(α) (c, 4.2 in CHCl3)+87.3
Flash Point 184.4°C
Solubility DMSO : ≥ 5.2 mg/mL (10.14 mM)
Vapor Presure 5.85E-16mmHg at 25°C
Appearance White to off-white (Solid)
Color White to Off-White
pKa 4.28±0.70(Predicted)
Storage Condition Sealed in dry,Store in freezer, under -20°C
Refractive Index 1.549
MDL MFCD03788777
In vitro study AKBA (Acetyl-11-keto-β-boswellic acid) 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). AKBA (Acetyl-11-keto-β-boswellic acid) significantly inhibited human colon adenocarcinoma growth, showing arrest of the cell cycle in G1-phase and induction of apoptosis. AKBA (Acetyl-11-keto-β-boswellic acid) 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 (Acetyl-11-keto-β-boswellic acid) treatment reduced phenotypic markers of mature adipocyte aP2, adiponectin and glut-4 in mature adipocytes.
In vivo study AKBA (Acetyl-11-keto-β-boswellic acid) 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. AKBA (Acetyl-11-keto-β-boswellic acid) 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. AKBA (Acetyl-11-keto-β-boswellic acid) 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.