VIP Antagonist是一种新型的、具有口服活性的血管活性肠肽（VIP）受体拮抗剂。
Cas No.:125093-93-8
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
VIP Antagonist is a novel, orally active vasoactive intestinal peptide (VIP) receptor antagonist[1-2]. VIP Antagonist can be used in research related to inflammation, cancer, antiviral applications, among others[3-4].
In vitro, NCI-H838 non-small cell lung cancer (NSCLC) cells were incubated with VIP Antagonist (10μM) and stimulated with VIP (100nM) for 2 weeks. VIP Antagonist significantly inhibited VIP-stimulated colony formation while reducing the elevation in cAMP levels induced by VIP[5]. Human glioblastoma cells (e.g., U87, U118, U373) were treated with VIP Antagonist (1–10μM) and PACAP-27 for 5 days. VIP Antagonist inhibited the PACAP-27-induced increases in cAMP and cytosolic Ca²⁺ and significantly suppressed cell proliferation[6].
In vivo, C57BL/6 and BALB/c mice received daily subcutaneous injections of VIP Antagonist (10μg per mouse) for one week, starting one day before infection with murine cytomegalovirus (mCMV). VIP Antagonist significantly improved the survival rate of infected mice, reduced viral load in the liver and lungs, and decreased inflammatory pathological damage in these organs[7]. C57BL/6 wild-type mice with colitis induced by drinking 2.5% dextran sodium sulfate (DSS) were treated with VIP Antagonist (0.1-1μM; 200μL) from day 0 to day 11. VIP Antagonist significantly alleviated the clinical symptoms, histopathological damage, and expression of pro-inflammatory cytokines associated with DSS-induced colitis[8].
References:
[1] Moody TW, Jensen RT, Fridkin M, et al. (N-stearyl, norleucine17)VIPhybrid is a broad spectrum vasoactive intestinal peptide receptor antagonist. J Mol Neurosci. 2002 Feb-Apr;18(1-2):29-35.
[2] Li JM, Petersen CT, Li JX, et al. Modulation of Immune Checkpoints and Graft-versus-Leukemia in Allogeneic Transplants by Antagonizing Vasoactive Intestinal Peptide Signaling. Cancer Res. 2016 Dec 1;76(23):6802-6815.
[3] Petersen CT, Li JM, Waller EK. Administration of a vasoactive intestinal peptide antagonist enhances the autologous anti-leukemia T cell response in murine models of acute leukemia. Oncoimmunology. 2017 Mar 16;6(5):e1304336.
[4] Moody TW, Hill JM, Jensen RT. VIP as a trophic factor in the CNS and cancer cells. Peptides. 2003 Jan;24(1):163-77.
[5] Moody TW, Zia F, Draoui M, et al. A vasoactive intestinal peptide antagonist inhibits non-small cell lung cancer growth. Proc Natl Acad Sci U S A. 1993 May 15;90(10):4345-9.
[6] Sharma A, Walters J, Gozes Y, et al. A vasoactive intestinal peptide antagonist inhibits the growth of glioblastoma cells. J Mol Neurosci. 2001 Dec;17(3):331-9.
[7] Li JM, Darlak KA, Southerland L, et al. VIPhyb, an antagonist of vasoactive intestinal peptide receptor, enhances cellular antiviral immunity in murine cytomegalovirus infected mice. PLoS One. 2013 May 27;8(5):e63381.
[8] Vu JP, Million M, Larauche M, et al. Inhibition of vasoactive intestinal polypeptide (VIP) induces resistance to dextran sodium sulfate (DSS)-induced colitis in mice. J Mol Neurosci. 2014 Jan;52(1):37-47.
VIP Antagonist是一种新型的、具有口服活性的血管活性肠肽（VIP）受体拮抗剂[1-2]。VIP Antagonist可用于炎症、癌症、抗病毒等相关研究[3-4]。
在体外，VIP Antagonist（10μM）与VIP（100nM）刺激非小细胞肺癌（NSCLC）细胞系NCI-H838 2周。VIP Antagonist显著抑制由VIP刺激的集落形成，同时降低由VIP引起的cAMP水平升高[5]。VIP Antagonist（1–10μM）与PACAP-27处理人胶质母细胞瘤细胞（如U87、U118、U373）5天。VIP Antagonist可抑制PACAP-27引起的cAMP升高和胞质Ca2+升高，并显著抑制细胞增殖[6]。
在体内，VIP Antagonist（10μg/只小鼠）每日一次皮下注射，用于处理C57BL/6和BALB/c小鼠，从感染巨细胞病毒（mCMV）前一天开始，持续一周。VIP Antagonist显著提高了感染小鼠的存活率，降低了肝脏和肺部的病毒载量，同时减少了这些器官的炎症病理损伤[7]。VIP Antagonist（0.1-1μM；200μL）用于处理饮用2.5%葡聚糖硫酸钠（DSS）诱导结肠炎的C57BL/6野生型小鼠，从第0天持续至第11天。VIP Antagonist显著减轻了DSS诱导的结肠炎临床症状、组织病理学损伤及促炎细胞因子表达[8]。
| Cell experiment [1]: | |
Cell lines | U87, U118, and U373 human glioblastoma cells |
Preparation Method | Cells were maintained in Dulbecco's Modified Eagle's Medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS) at 37°C, 5% CO₂. For the clonogenic assay, cells were treated with VIP Antagonist (10μM) in soft agar containing 0.3% agarose, 0.1% BSA, and 5% FBS. |
Reaction Conditions | 10μM; 2 weeks. |
Applications | VIP Antagonist significantly inhibited the proliferation of glioblastoma cells by reducing colony formation in a concentration-dependent manner. VIP Antagonist also functioned as a PAC1 receptor antagonist, inhibiting PACAP-27-induced cAMP elevation and cytosolic Ca²⁺ increase in these cells. |
| Animal experiment [2]: | |
Animal models | C57BL/6 mice and BALB/c mice |
Preparation Method | Mice were administered daily subcutaneous injections of VIP Antagonist (10μg per mouse) for 1 week, starting one day prior to intraperitoneal infection with murine cytomegalovirus (mCMV). Mice were monitored for survival, and tissues (e.g., liver, lung, spleen) were harvested at various time points post-infection for analysis of viral load, histopathology, and immune cell populations. |
Dosage form | 10μg per mouse; s.c.; Daily injections for 7 days. |
Applications | VIP Antagonist administration significantly enhanced survival and reduced viral load in the liver and lungs of mCMV-infected mice. VIP Antagonist decreased inflammation and tissue damage (e.g., fewer intranuclear inclusions, necrotic foci) in the liver and lung. VIP Antagonist treatment increased the numbers of effector/memory CD8+ T cells and mature NK cells, while decreasing the percentage of splenic regulatory T cells (Treg). VIP Antagonist prevented the up-regulation of PD-1 on activated CD8+ T cells and PD-L1 on dendritic cells (DCs), and enhanced the expression of co-stimulatory molecules (CD80, CD86) and MHC-II on conventional and plasmacytoid DCs. VIP Antagonist increased type-I interferon synthesis and the numbers of IFN-γ- and TNF-α-expressing NK cells and T cells. |
References: | |
| Cas No. | 125093-93-8 | SDF | |
| 分子式 | C154H257N49O40S | 分子量 | 3467.06 |
| 溶解度 | Soluble in DMSO | 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 | 288.4 μL | 1.4421 mL | 2.8843 mL |
| 5 mM | 57.7 μL | 288.4 μL | 576.9 μL |
| 10 mM | 28.8 μL | 144.2 μL | 288.4 μL |
| 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。
Quality Control & SDS
- View current batch:
- Purity: >99.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet