Leukotriene B5
(Synonyms: LTB5) 目录号 : GC41107
A leukotriene
Cas No.:80445-66-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Leukotriene B5 (LTB5) is a leukotriene with diverse biological activities. It is a metabolite of eicosapentaenoic acid formed through the 5-lipoxygenase (5-LO) pathway. LTB5 increases contraction of bullfrog lung strips ex vivo in a concentration-dependent manner. In vivo, LTB5 (100 nM) reduces tumor volume in mice injected with Tm1 murine melanoma cells. LTB5 also elicits chemokinesis and lysosomal enzyme release from polymorphonuclear leukocytes (PMNLs) 20- to 30-fold less, and induces platelet aggregation 8-fold less, potently than LTB4 .
| Cas No. | 80445-66-5 | SDF | |
| 别名 | LTB5 | ||
| Canonical SMILES | CC/C=C\C/C=C\C[C@@H](O)/C=C/C=C/C=C\[C@@H](O)CCCC(O)=O | ||
| 分子式 | C20H30O4 | 分子量 | 334.5 |
| 溶解度 | DMF: >50 mg/ml (per Rao Maddipati),DMSO: >50 mg/ml (per Rao Maddipati),Ethanol: >50 mg/ml (per Rao Maddipati),PBS pH 7.2: >1 mg/ml (from 13(S)-HODE) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.9895 mL | 14.9477 mL | 29.8954 mL |
| 5 mM | 0.5979 mL | 2.9895 mL | 5.9791 mL |
| 10 mM | 0.299 mL | 1.4948 mL | 2.9895 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Leukotriene B3, leukotriene B4 and Leukotriene B5; binding to leukotriene B4 receptors on rat and human leukocyte membranes
Prostaglandins 1986 Oct;32(4):503-16.PMID:3025936DOI:10.1016/0090-6980(86)90033-x.
Specific high-affinity binding sites for [3H]-leukotriene B4 have been identified on membrane preparations from rat and human leukocytes. The rat and human leukocyte membrane preparations show linearity of binding with increasing protein concentration, saturable binding and rapid dissociation of binding by excess unlabelled leukotriene B4. Dissociation constants of 0.5 to 2.5 nM and maximum binding of 5000 fmoles/mg protein were obtained for [3H] leukotriene B4 binding to these preparations. Displacement of [3H]-leukotriene B4 by leukotriene B4 was compared with displacement by leukotriene B3 and Leukotriene B5 which differ from leukotriene B4 only by the absence of a double bond at carbon 14 or the presence of an additional double bond at carbon 17, respectively. Leukotriene B3 was shown to be equipotent to leukotriene B4 in ability to displace [3H]-leukotriene B4 from both rat and human leukocyte membranes while Leukotriene B5 was 20-50 fold less potent. The relative potencies for the displacement of [3H]-leukotriene B4 by leukotrienes B3, B4 and B5 on rat and human leukocyte membranes were shown to correlate well with their potencies for the induction of the aggregation of rat leukocytes and the chemokinesis of human leukocytes.
Catabolism of Leukotriene B5 in humans
J Lipid Res 1990 Oct;31(10):1831-8.PMID:1964169doi
Human neutrophils, enriched by dietary supplementation with eicosapentaenoic acid, form leukotriene (LT)B5 in addition to LTB4 upon stimulation. LTB5 is one order of magnitude less biologically active than the potent chemokinetic and chemoattractant LTB4. Catabolites of LTB5 have not yet been characterized in vitro and ex vivo. It is unknown whether catabolism of LTB5 interferes with catabolism of LTB4. This report describes catabolism of LTB5 to 20-OH-LTB5, which in turn is catabolized to 20-COOH-LTB5. The structures of the two catabolites were established by UV-absorbance, behavior on reverse-phase high-performance liquid chromatography, enzymatic analysis of human neutrophils, and gas chromatography-mass spectrometry. In vitro, formation of LTB4 was delayed and formation of its catabolites was depressed by exogenous eicosapentaenoic acid. By supplementing the diet of six volunteers with 5 g eicosapentaenoic acid/day for 7 days, eicosapentaenoic acid quadrupled in neutrophil phospholipid fatty acids. Consequently, LTB5, 20-OH-LTB5, and 20-COOH-LTB5 were detected ex vivo. In contrast to the findings in vitro, however, levels of LTB4, 20-OH-LTB4, and 20-COOH-LTB4 were unaltered by the dietary intervention. Thus, in vitro, but not ex vivo, addition of eicosapentaenoic acid, and subsequent formation of LTB5, impeded catabolism of proinflammatory LTB4.
Inhibition by Leukotriene B5 of leukotriene B4-induced activation of human keratinocytes and neutrophils
J Invest Dermatol 1987 May;88(5):555-8.PMID:2437212DOI:10.1111/1523-1747.ep12470151.
Leukotriene B5 (LTB5) that is generated enzymatically from eicosapentaenoic acid (EPA), was compared with arachidonic acid-derived LTB4 for its DNA synthetic effect on cultured human epidermal keratinocytes and for its chemokinetic effect on human blood neutrophils. Leukotriene B5 was much less potent than LTB4 in stimulating DNA synthesis and in inducing chemokinesis. Furthermore, the maximum response to LTB5 was only a mean of 38% that of LTB4 for mitogenesis and 70% that of LTB4 for chemokinesis. At an optimally active concentration of LTB4 (10(-10) M) the addition of LTB5 suppressed the enhancement by LTB4 of DNA synthesis in keratinocytes by a mean of 21%, 33%, and 54%, respectively, at 10(-9) M, 10(-8) M, and 10(-7) M LTB5. Leukotriene B5 inhibited to a lesser extent the maximum neutrophil chemokinetic response elicited by 10(-10) M LTB4 with mean inhibition of 10%, 20%, and 18%, respectively, by 10(-9) M, 10(-8) M, 10(-7) M LTB5; LTB5 was without effects on N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)-elicited neutrophil chemokinesis and on thrombin-stimulated keratinocyte DNA synthesis. The dietary introduction of n-3 fatty acids, such as EPA, may reduce the epidermopoiesis and neutrophil migration evoked by LTB4 through decreases in generation of LTB4 and the capacity of LTB5 to inhibit the effects of LTB4.
Leukotriene B5 is formed in human neutrophils after dietary supplementation with icosapentaenoic acid
Proc Natl Acad Sci U S A 1985 Mar;82(5):1540-3.PMID:2983350DOI:10.1073/pnas.82.5.1540.
Incorporation and conversion of icosapentaenoic acid (20:5, n - 3) by human polymorphonuclear leukocytes were studied in volunteers (n = 6) ingesting a normal Western diet supplemented with icosapentaenoic acid (approximately equal to 4 g daily). Ingestion of icosapentaenoic acid leads to formation of biologically less active Leukotriene B5 (LTB5) from polymorphonuclear leukocytes (PMNL) stimulated with ionophore A23187. LTB5 was identified on HPLC by UV absorption and by GC/MS and showed a behavior identical to that of in vitro synthesized LTB5 produced by incubation of human PMNL with icosapentaenoic acid. The ratio of icosapentaenoic acid/arachidonic acid (20:4, n - 6) in cellular phospholipids increased from 0.045 during control to 0.28 after the supplemented period. LTB5 increased from undetectable values to 70.2 +/- 18.7 pmol of LTB5 per 10(7) PMNL during the experimental period. Synthesis of LTB4 did not change significantly (control, 218.8 +/- 89.1; icosapentaenoic acid-enriched diet, 253.6 +/- 18.7 pmol per 10(7) PMNL). The ratio of LTB4/LTB5 corresponded to the ratio of arachidonic acid/icosapentaenoic acid in PMNL phospholipids. Our findings prove that LTB5, which is 10 to 30 times less potent than LTB4 to cause aggregation, chemotaxis, and degranulation of PMNL, can be formed in vivo in man after dietary icosapentaenoic acid. This may modify the contribution of leukotrienes in processes in which these metabolites are of pathogenetic relevance.
Leukotriene B4 and Leukotriene B5 have binding sites on lung membranes and cause contraction of bullfrog lung
J Pharmacol Exp Ther 1992 Dec;263(3):1111-7.PMID:1335056doi
Leukotriene (LT)B4 and LTB5 cause contraction of isolated bullfrog lung. LTB4 receptors were characterized in membranes prepared from bullfrog lung. Binding of [3H]LTB4 was maximal at 5 min and was reversible with the addition of 1000-fold excess LTB4. Scatchard analysis indicated a single class of binding sites with a Kd of 2.22 nM and a Bmax of 1228.86 fmol/mg protein. The Kd and the Bmax values in the presence of guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S) were 2.76 nM and 1289.61 fmol/mg protein, respectively. The Ki values for LTB4, LTB5 and 20(OH)-LTB4 were 5.5, 30.5 and 144.0 nM, respectively, whereas 20(COOH)-LTB4 was ineffective in preventing binding of [3H] LTB4 from 10(-9) to 10(-5) M. The peptide leukotrienes LTC4, LTD4 and LTE4 failed to inhibit the specific binding of [3H]LTB4. GTP gamma S in concentrations from 10(-10) to 10(-4) M did not affect the binding of 5 nM [3H]LTB4. Neither the mammalian LTD4 antagonist LY171883 nor the mammalian LTB4 antagonist LY255283 was an effective competitor for the bullfrog lung LTB4 receptor. In addition, sulfhydryl-modifying reagents NEM and PCMP did not affect LTB4 binding as they do in mammalian membrane preparations. The LTB4 receptor shows some differences from the described mammalian receptor. The cell type containing the LTB4 receptor remains to be determined.