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Detail of > 121250-47-3

  • CAS Number:
  • 121250-47-3
  • Name:
  • 9,11-Linoleic acid

  • Formula:
  • C18H32O2
  • Molecular Structure:
  • Synonyms:
  • Conjugated Linoleic Acid;Octadecadienoic acid;9,11(or 10,12)-Octadecadienoic acid;
  • Molecular Weight:
  • 280.44
  • Density:
  • 0.911 g/cm3
  • Boiling Point:
  • 412.1 °C at 760 mmHg
  • Flash Point:
  • 307.3 °C
  • Deleted CAS:
  • 342889-37-6
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121250-47-3 9,11-Linoleic acid

CLA
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CAS No. 

121250-47-3 9,11-Linoleic acid

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CAS No. 

121250-47-3 9,11-Linoleic acid

Items Specification Test Results Appearance White Powder Complied Oil Content 20%-30% 21.10% CLA 18:2 Conjugated 78-82% 79.10% Bulk Density 0.4g/ml-0.6g/ml 0.56g/ml Loss on Drying 5.0% ma
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  • Address:NO.2 Minjiang Road, Qingdao,China
Min. Order:25 Kilogram

CAS No. 

121250-47-3 9,11-Linoleic acid

Chemistry: TOXICITY: SAFETY: Production: Others: Name:Conjugated Linoleic Acid CAS Number:121250-47-3 Molecular Formula:C18H32O2 Molecular Weight:280.44 Density:0.911g/cm3 Boiling Point:412.1°Cat760mmHg Flash Point:307.3°C
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  • Address:No.450, Zeng Cuo An

CAS No. 

121250-47-3 9,11-Linoleic acid

25kg/drum pharma grade assay:99%
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CAS No. 

121250-47-3 9,11-Linoleic acid

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121250-47-3 9,11-Linoleic acid

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    Reference

    Effects of dietary conjugated linoleic acid on the productivity of laying hens and egg quality during refrigerated storage
    Effects of dietary conjugated linoleic acid on the productivity of laying hens and egg quality during refrigerated storage. Shang, X. G.; Wang, F. L.; Li, D. F.; Yin, J. D.; Li, J. Y. (Animal Science and Technology College, China Agricultural University, Beijing 100094, Peop. Rep. China). Poultry Science, 83(10), 1688-1695 (English) 2004 Poultry Science Association, Inc. CODEN: POSCAL. ISSN: 0032-5791. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) Section cross-reference(s): 17 Five hundred and four 40-wk-old Brown Dwarf hens (1.51 ± 0.08 kg BW) were fed corn-soybean meal diets contg. 0, 1, 2, 3, 4, 5, or 6% conjugated linoleic acid (CLA) for 56 d to measure the effects of dietary CLA on laying hen productivity and egg quality during refrigerated storage.There are some reagents with their cas registry numbers 121250-47-3 and 7440-09-7 are used in this study. Four hens were placed in 1 cage, and 3 cages were grouped as 1 replicate resulting in 6 replicates per treatment. After feeding the exptl. diets for 11 d, eggs were collected to det. the fatty acid compn. of egg yolks. From d 12 to 18, eggs from hens fed diets contg. 0, 2, 4, and 6% CLA diets were stored at 4°C for up to 28 d. At designated times (1, 14, or 28 d), eggs were taken, broken, and shelled to evaluate water content, pH, and ion concn. Firmness of hard-cooked egg yolk was also detd. With increased dietary CLA, feed intake, BW gain, rate of egg prodn., egg wt., and feed efficiency all decreased linearly (P < 0.01). The wt. of the yolk, albumen, and shell decreased linearly (P < 0.01) with increasing dietary CLA. Concn. of CLA in the yolk lipids increased quadratically (P < 0.01), with increasing dietary CLA. Concurrent increases (P < 0.01) in the concn. of myristic, palmitic, and stearic acids and decreases (P < 0.01) in oleic, linoleic, linolenic, and arachidonic acids in egg yolk lipids were obsd. Days of storage and CLA (P < 0.01) increased yolk firmness. Egg yolk water content and pH increased with storage and CLA content (P < 0.01). Corresponding decreases were obsd. in albumen pH. Regardless of dietary treatment, the concns. of Na, K, and Mg in egg yolks increased with longer storage time. At 28 d of storage, there was a linear (P < 0.01) increase in Na, K, and Mg content in egg yolks as dietary CLA increased. In contrast to the egg yolk, the concns. of Na, K, and Mg in egg albumen decreased with storage time. On d 28, there was a linear decrease (P < 0.01) in the Na content of albumen with increasing CLA. This study suggests that the greater firmness of CLA-fed eggs might be related to the change of pH, water content, and ion concns. during refrigerated storage. .
    Activation of PPAR g and d by conjugated linoleic acid mediates protection from experimental inflammatory bowel disease
    Activation of PPAR g and d by conjugated linoleic acid mediates protection from experimental inflammatory bowel disease. Bassaganya-Riera, Josep; Reynolds, Kathryn; Martino-Catt, Susan; Cui, Yongzhi; Hennighausen, Lothar; Gonzalez, Frank; Rohrer, Jurg; Benninghoff, Alejandro Uribe; Hontecillas, Raquel (Laboratory of Nutritional Immunology & Molecular Nutrition, Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA). Gastroenterology, 127(3), 777-791 (English) 2004 Elsevier Inc. CODEN: GASTAB. ISSN: 0016-5085. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) Section cross-reference(s): 14 Background & Aims: The mol. targets for the protective actions of conjugated linoleic acid (CLA) on exptl. inflammatory bowel disease (IBD) are unknown. We used a loss-of-function approach to investigate whether CLA ameliorated colitis through a peroxisome proliferator-activated receptor g (PPAR g)-dependent mechanism.Some commonly used reagents like 121250-47-3 and 2540-56-9 are used in this experiment. Methods: The expression of PPAR g, d, and their target genes in the colon of mice fed control or CLA-supplemented diets was assayed after a 7-day dextran sodium sulfate (DSS) challenge by quant. real-time polymerase chain reaction (PCR). Addnl., nuclear factor-k B (NF-kB) p65 activation was quantified in the colon. To det. the involvement of PPAR g in the mechanism of action of CLA directly, specific deletions of PPAR g in the colon were performed in mice by using the Cre-lox recombination system. Colonic PPAR g null mice and wild-type littermates were fed either a CLA-supplemented or a control diet for 42 days and challenged with 2.5% DSS. The therapeutic efficacy of CLA also was examd. by using the CD4+CD45RBhi transfer colitis model. Results: CLA induced PPAR g and d, transcriptionally modulated PPAR g and d-responsive gene clusters involved in lipid metab. (uncoupling protein [UCP]1, UCP3, PPAR g coactivator 1a [PGC-1a], and CD36) and epithelial cell maturation (Gob-4 and Keratin 20). Addnl., CLA repressed tumor necrosis factor a (TNF-a) expression and NF-kB activation while inducing the immunoregulatory cytokine transforming growth factor b 1 (TGF-b1). Clin., CLA ameliorated DSS- and CD4+-induced colitis. Loss of the PPAR g gene in the colon abrogated the beneficial effects of CLA in DSS colitis. Conclusions: Our studies provide mol. evidence in vivo, suggesting that CLA ameliorates colitis through a PPAR g-dependent mechanism. .

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