Aspartyl-alanyl-diketopiperazine
(Synonyms: DA-DKP) 目录号 : GC35410
Aspartyl-alanyl-diketopiperazine (DA-DKP) 是一种免疫调节分子，由人血白蛋白的 N 端裂解和环化产生，通过与 T 淋巴细胞无反应相关的分子途径调节炎症免疫反应。
Cas No.:110954-19-3
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Aspartyl-alanyl-diketopiperazine (DA-DKP) is an immunomodulatory molecule generated by cleavage and cyclization from the N-terminus of human albumin and can modulate the inflammatory immune response through a molecular pathway implicated in T- lymphocyte anergy[1][2].
[1]. Bar-Or D, et al. Dipeptidyl peptidase IV activity in commercial solutions of human serum albumin. Anal Biochem. 2013 Oct 1;441(1):13-7. [2]. Shimonkevitz R, et al. A diketopiperazine fragment of human serum albumin modulates T-lymphocyte cytokine production through rap1. J Trauma. 2008 Jan;64(1):35-41.
| Cas No. | 110954-19-3 | SDF | |
| 别名 | DA-DKP | ||
| Canonical SMILES | O=C(O)C[C@@H](C(N[C@H]1C)=O)NC1=O | ||
| 分子式 | C7H10N2O4 | 分子量 | 186.17 |
| 溶解度 | DMSO: 125 mg/mL (671.43 mM) | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 5.3714 mL | 26.8572 mL | 53.7143 mL |
| 5 mM | 1.0743 mL | 5.3714 mL | 10.7429 mL |
| 10 mM | 0.5371 mL | 2.6857 mL | 5.3714 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。
A diketopiperazine fragment of human serum albumin modulates T-lymphocyte cytokine production through rap1
J Trauma 2008 Jan;64(1):35-41.PMID:18188096DOI:10.1097/TA.0b013e3181589ff9.
Background: Aspartyl-alanyl- diketopiperazine (DA-DKP) is generated by cleavage and cyclization from the N-terminus of human albumin during the preparation of commercial serum albumin product. Antigen-stimulated human T lymphocytes produce significantly lower quantities of interferon-gamma and tumor necrosis factor-alpha after stimulation in vitro in the presence of DA-DKP. Methods: T lymphocytes activated in the presence of DA-DKP were analyzed by pull-down western blot assay for the activation of the guanosine triphosphatase Rap1 and by quantitative immunoassay for the phosphorylated transcription factors ATF-2 (activating transcription factor-2) and c-jun, which regulate the production of interferon-gamma and tumor necrosis factor-alpha. Results: Exposure of human T lymphocytes to DA-DKP resulted in increased levels of active Rap1 and decreased activation factors relevant to the T-cell receptor signal transduction pathway and subsequently, decreased phosphorylated ATF-2 and c-jun expression. Conclusion: The cyclized N- terminal fragment of human serum albumin, DA-DKP, can modulate the inflammatory immune response through a molecular pathway implicated in T- lymphocyte anergy.
Commercial human albumin preparations for clinical use are immunosuppressive in vitro
Crit Care Med 2006 Jun;34(6):1707-12.PMID:16625113DOI:10.1097/01.CCM.0000217923.53680.4C.
Objective: We previously reported significant variations in oxidation status and molecular length among sources and lots of human serum albumin (HSA) commercial preparations intended for clinical use. In this report, we investigated what effect the presence of HSA products have on the immune response in vitro. Design: Laboratory study. Setting: Trauma research basic science laboratory. Subjects: Activated human peripheral blood mononuclear cells. Interventions: Six commercial HSA preparations were tested for their effect on cytokine release from activated human peripheral blood mononuclear cells (PBMCs) and T-lymphocytes. Mass spectrometry analysis of Aspartyl-alanyl diketopiperazine (DA-DKP) content of HSA and percentage of HSA having lost its amino terminal dipeptide aspartyl alanyl (HSA-DA) were correlated. Measurements and main results: Human PBMCs were cultured in the presence of six commercial HSA preparations and activated via the T-cell receptor complex. A cloned T-lymphocyte cell line, activated with specific antigen, was also cultured with both synthetic DA-DKP and small molecular weight extracts from the commercial HSA tested. Supernatants were quantified by enzyme-linked immunosorbent assay for interferon-gamma and tumor necrosis factor-alpha content. DA-DKP was extracted from HSA by centrifugal filters and quantified by anion exchange liquid chromatography coupled to negative electrospray ionization mass spectrometry. HSA species were determined by reverse phase liquid chromatography coupled to positive electrospray ionization, time of flight mass spectrometry. All HSA preparations significantly inhibited the in vitro production of interferon-gamma and tumor necrosis factor-alpha by activated PBMCs. DA-DKP was detected in all HSA sources at concentrations ranging between 42.0 and 79.6 microM. A synthetic form of DA-DKP possessed similar immunosuppressive qualities in a dose-dependent manner on T lymphocytes. Conclusions: DA-DKP was present in significant concentrations in all HSA sources tested and was partially responsible for the immunosuppressive effects of HSA on activated PBMCs and T-lymphocytes in vitro. In view of these findings, administering HSA to immunocompromised critically ill patients might be reevaluated.