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Detail of "870-93-9"

  • CAS Number:
  • 870-93-9
  • Name:
  • Butanoic acid,4,4'-dithiobis[2-amino-, (2R,2'R)-rel-

  • Superlist Name:
  • DL-Homocystine
  • Molecular Structure:
  • Formula:
  • C8H16N2O4S2
  • Molecular Weight:
  • 268.35
  • Synonyms:
  • Butanoicacid, 4,4'-dithiobis[2-amino-, (R*,R*)-(?à)-;Butyric acid, 4,4'-dithiobis[2-amino-, DL- (8CI);DL-4,4'-Dithiobis(2-aminobutyric acid);NSC 226570;
  • EINECS:
  • 212-803-5
  • Density:
  • 1.443 g/cm3
  • Melting Point:
  • ≥300 °C
  • Boiling Point:
  • 507.6 °C at 760 mmHg
  • Flash Point:
  • 260.8 °C
  • Appearance:
  • white to slightly beige solid

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CAS No.870-93-9 DL-Homocystine

Assay:99%  Package:in 25kgs car...Storage:normal condi...  Transportation:non dangerou...  Application:intermediate...

Min. Order:25Kilogram

Supplier:Nice-synth Chemical Industry Ltd. [ China (Mainland)]

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910Integral
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Tel:+86-(574)-81110986

Address:No. 411, Building 3, Wante Business Centre, Hi-tech Zone, Ningbo

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CAS No.870-93-9 DL-Homocystine

Assay:98%  Appearance:White powder

Supplier:Taiyuan RHF CO., ltd. [ China (Mainland)]

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2160

Tel:0351-7436719

Address:Shuangta South Alley 46,2-1, YingZe Area,Taiyuan, ShanXi

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CAS No.870-93-9 DL-Homocystine

Assay:98%

Supplier:Hangzhou Dayangchem Co., Ltd. [ China (Mainland)]

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ISO 3875Integral
3875

Tel:+86-571-88938639

Address:B/2601 Fuli Building, 328# WenEr Rd. Hangzhou City 310012 China

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CAS No.870-93-9 DL-Homocystine

Supplier:KINHENG CHEMICAL(SHANGHAI)CO., LTD. [ China (Mainland)]

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Tel:+8621-60490170

Address:Room401, No.28,Lane 189, Yangshupu Rd. Shanghai, China.

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CAS No.870-93-9 DL-Homocystine

Supplier:Afine Chemicals Limited [ China (Mainland)]

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930

Tel:+86-571-85134551

Address:No. 206 Zhen Hua Road, Hangzhou 310030, Zhejiang, China

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CAS No.870-93-9 DL-Homocystine

98%

Supplier:Zheda Panaco Chemical Engineering Co., Ltd. [ China (Mainland)]

560Integral
560

Tel:+86-571-87982106

Address:18 Shihushan, Yugu Rd., Hangzhou 310027, China

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CAS No.870-93-9 DL-Homocystine

Appearance: white powder,assay:99%Min

Supplier:Hangzhou Shinyang Samwoo Fine Chemical Co.,ltd [ China (Mainland)]

414Integral
414

Tel:+86-13819496681

Address:Rm708 Deep blue Plaza, No.203 Chaohui Rd,Hangzhou,china

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CAS No.870-93-9 DL-Homocystine

Supplier:HangZhou Puris Biotechnology Ltd [ China (Mainland)]

10Integral
10

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Address:Wantang RD262, Hangzhou,Zhejiang P.R,China

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CAS No.870-93-9 DL-Homocystine

Supplier:Zhengzhou Alfachem Co., Ltd. [ China (Mainland)]

600Integral
600

Tel:0371-55616343

Address:zhengzhou

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CAS No.870-93-9 DL-Homocystine

Supplier:Sequoia Research Products Limited [ United Kingdom]

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540

Tel:+44 7802 291086

Address:RG8 7AP,

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CAS No.870-93-9 DL-Homocystine

Supplier:Research Organics, Inc. [ United States]

610Integral
610

Tel:216-883-8025

Address:4353 East 49th Street Cleveland, OH. 44125

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CAS No.870-93-9 DL-Homocystine

Supplier:Nanjing Honorline Co., Ltd. [ China (Mainland)]

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450

Tel:86-25-84798606,84798607

Address:Room 1103, A, Chengkai mansion, 198# Hongwulu, Nanjing, China

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CAS No.870-93-9 DL-Homocystine

Supplier:Beijing Hengrun Weiyuan Biotechnologies,. Inc. [ China (Mainland)]

670Integral
670

Tel:+86-570-3081766

Address:Room 624A No.58, Liangguan Rd, Fangshan, Beijing, China

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Reference

Anti-inflammatory drugs in experimental atherosclerosis
Anti-inflammatory drugs in experimental atherosclerosis. Part 3. Evaluation of the atherogenicity of homocystine in rabbits. Makheja, A. N.; Bombard, A. T.; Randazzo, R. L.; Bailey, J. M. (Dep. Biochem., George Washington Univ. Sch. Med., Washington, D. C., USA). Atherosclerosis (Shannon, Irel.), 29(1), 105-12 (English) 1978. CODEN: ATHSBL. ISSN: 0021-9150. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) Section cross-reference(s): 1 Dietary administration of DL-homocysteine thiolactone-HCl [6038-19-3], DL-homocystine [870-93-9], or DL-homocysteic acid [504-33-6] to rabbits for 12 wk only slightly increased plasma levels of homocystine, did not affect serum cholesterol [57-88-5] levels, did not alter the pattern of collagen-induced platelet aggregation, and induced no atherosclerotic plaque formation. The absence of pathol. effects was consistent with the rapid clearance of i.v. injected homocystine from rabbit plasma. Thus, the rabbit is not an acceptable exptl. model for study of the thromboatherogenic effects of homocystine reported for humans and some other animals.
Effect of methotrexate with 5-methyltetrahydrofolate rescue and dietary homocystine on survival of leukemic mice and on concentrations of liver adenosylamino acids
Effect of methotrexate with 5-methyltetrahydrofolate rescue and dietary homocystine on survival of leukemic mice and on concentrations of liver adenosylamino acids. Hilton, Mary A.; Hoffman, Jerald L.; Sparks, Margaret K. (Sch. Med., Univ. Louisville, Louisville, KY 40292, USA). Cancer Res., 43(11), 5210-16 (English) 1983. CODEN: CNREA8. ISSN: 0008-5472. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The survival time of DBA/2 mice bearing methionine [63-68-3]-dependent L1210 or L5178Y leukemia cells was increased by i.p. administration of LDs of methotrexate [59-05-2] (5 daily doses of 25 mg/kg) followed by rescue with 5-methyltetrahydrofolate [134-35-0] (5 daily doses of 20 mg/kg).Several substances with their cas registry numbers 979-92-0 and 29908-03-0 may be metioned in this study. The mice were maintained on a semipurified choline and cyst(e)ine-free diet contg. 0.32% L-methionine. The survival time of the treated animals bearing L5178Y cells, but not those bearing L1210 cells, was further increased by substitution of 0.86% DL-homocystine [870-93-9] for the methionine in the diet. The effects of both diets in mice treated with methotrexate and 5-methyltetrahydrofolate, singly and in combination, were examd. on the concns. of S-adenosylmethionine [29908-03-0] and S-adenosylhomocysteine [979-92-0] in the liver, a tissue highly active in the metab. of these amino acids. The substitution of homocystine for methionine in the diet of untreated animals led to an increase in S-adenosylhomocysteine and decrease in S-adenosylmethionine in the liver which was not further altered by methotrexate. .
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