Roquinimex
(Synonyms: 罗喹美克,Linomide; FCF89; ABR212616) 目录号 : GC37555
An immunomodulator with diverse biological activities
Cas No.:84088-42-6
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: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Roquinimex is an immunomodulator with diverse biological activities.1,2,3,4 In vivo, roquinimex (80 mg/kg) increases the number of myocardial MHC class II-expressing cells, the ratio of cytotoxic to helper T cells, and survival and decreases necrotic lesion area in a mouse model of murine coxsackievirus B3-induced myocarditis.1 It induces IFN-γ production, reduces TNF-α and IL-1β production, prevents the development of proteinuria, and ameliorates nephritis in a mouse model of chronic graft versus host disease (GVHD).2 Roquinimex (300 mg/kg) decreases colonic myeloperoxidase (MPO) activity and mucosal damage in a mouse model of colitis induced by dextran sulfate .3 It also decreases tumor weight and tumor blood flow in a von Hippel-Lindau (VHL) type 2a paraganglioma mouse xenograft model.4
1.Ilb?ck, N.G., Fohlman, J., Slorach, S., et al.Effects of the immunomodulator LS 2616 on lymphocyte subpopulations in murine coxsackievirus B3 myocarditisJ. Immunol.142(9)3225-3228(1989) 2.Xiao, Z.-Y., Zhou, W.-X., Zhang, Y.-X., et al.Roquinimex-mediated protection effect on the development of chronic graft-versus-host disease in mice is associated with induction of Th1 cytokine production and inhibition of proinflammatory cytokine productionLife Sci.81(19-20)1403-1410(2007) 3.Liu, Q., Wang, Y., Wan, M.X., et al.Roquinimex inhibits dextran sodium sulfate-induced murine colitisInflamm. Res.52(2)64-68(2003) 4.Gross, D.J., Reibstein, I., Weiss, L., et al.The antiangiogenic agent linomide inhibits the growth rate of Von Hippel-Lindau paraganglioma xenografts to miceClin. Cancer Res.5(11)3669-3675(1999)
| Cas No. | 84088-42-6 | SDF | |
| 别名 | 罗喹美克,Linomide; FCF89; ABR212616 | ||
| Canonical SMILES | O=C(C1=C(O)C2=C(N(C)C1=O)C=CC=C2)N(C)C3=CC=CC=C3 | ||
| 分子式 | C18H16N2O3 | 分子量 | 308.33 |
| 溶解度 | DMSO: ≥ 83.3 mg/mL (270.17 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 | 3.2433 mL | 16.2164 mL | 32.4328 mL |
| 5 mM | 0.6487 mL | 3.2433 mL | 6.4866 mL |
| 10 mM | 0.3243 mL | 1.6216 mL | 3.2433 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。
Roquinimex (Linomide) vs placebo in AML after autologous bone marrow transplantation
Bone Marrow Transplant 2000 Jun;25(11):1121-7.PMID:10849523DOI:10.1038/sj.bmt.1702411.
Roquinimex, Linomide, a quinoline derivative with pleiotropic immunomodulatory activity, has previously been shown to enhance natural killer (NK) cell number and activity after ABMT in patients with AML. In this study 278 AML patients in remission were randomized to receive Roquinimex 0.2 mg/kg body weight or placebo twice weekly for 2 years following ABMT. Out of 139 patients in each group, 109 Roquinimex patients and 108 placebo patients were in their first CR. Median age at inclusion was 41 years for Roquinimex patients and 39 years for placebo patients. Twelve patients in each group had their marrow purged prior to reinfusion. Relapse and death were study endpoints. Surviving patients were followed for 2.6 to 6. 9 years. The total number of relapses was 60 in the Roquinimex group and 63 in the placebo group (not significant). Leukemia-free and overall survivals were similar in the two groups. Recovery of platelet counts was significantly delayed in the Roquinimex group as compared to placebo. No other significant differences regarding toxicity parameters were recorded. In conclusion, previous findings on NK cells could not be confirmed and the study showed no benefit for Roquinimex over placebo regarding relapse or survival following ABMT for AML in remission.
Roquinimex-mediated protection effect on the development of chronic graft-versus-host disease in mice is associated with induction of Th1 cytokine production and inhibition of proinflammatory cytokine production
Life Sci 2007 Oct 27;81(19-20):1403-10.PMID:17950363DOI:10.1016/j.lfs.2007.08.044.
Roquinimex is an immunomodulator that can effectively inhibit the development of several autoimmune diseases in animal models, but the mechanism is still unknown. In this study, we investigated the effect of Roquinimex on chronic graft-versus-host disease (GVHD) in mice, a well-established model for human systemic lupus erythematosus (SLE). Oral administration of Roquinimex significantly suppressed the development of proteinuria and ameliorated nephritis symptoms in chronic GVHD mice. In addition, renal histopathology and immunohistochemistry studies revealed reduced glomerulonephritis and decreased IgG deposition in chronic GVHD mice treated with Roquinimex. Chronic GVHD is characterized by a predominance of Th2 cytokines, and proinflammatory cytokines that also play an important role in the pathology of tissue damage. Therefore, we focused on the effect of Roquinimex on cytokine production. Chronic GVHD mouse splenocytes exhibited severely reduced interferon (IFN)-gamma production in response to Concanavalin (Con A) stimulation and an overt Th2 skewness. Roquinimex treatment, however, induced IFN-gamma production and restored the Th1/Th2 cytokine balance, although only a minimal effect of Roquinimex on interleukin (IL)-4 secretion was observed. The production of the proinflammatory cytokines TNF-alpha and IL-1 beta by peritoneal macrophages from lipopolysaccharide (LPS)-treated GVHD mice was significantly inhibited by Roquinimex treatment. These data suggested that the beneficial effect of Roquinimex on lupus might, at least in part, result from a restoration of Th1/Th2 cytokine balance and inhibition of inflammatory cytokine production.
Metabolism of Roquinimex in mouse and rat: an in vitro/in vivo comparison
Xenobiotica 2000 Apr;30(4):371-80.PMID:10821166DOI:10.1080/004982500237578.
1. In vitro studies with Roquinimex, an immuno-modulator, in liver microsomes from mouse and rat were conducted to evaluate the primary metabolism and compare the metabolite pattern as well as the rate of metabolism with the in vivo pharmacokinetics of the compound in these two species. 2. In the presence of NADPH, Roquinimex was metabolized to six primary metabolites (R1-6) by liver microsomes from mouse and rat. The formation of these metabolites was qualitatively similar in both species, and was greatly enhanced by pretreatment with PCN, an inducer of cytochrome P4503A. 3. The identification of the R1-6 demonstrated that Roquinimex had been hydroxylated and demethylated. Hydroxylation at different sites of the quinoline moiety was the dominating reaction in both species. 4. Comparison of the resulting microsomal intrinsic clearance of 0.3 micromol mg(-1) protein min(-1) in mouse liver microsomes, versus 0.03 micromol mg(-1) protein min(-1) in rat liver microsomes demonstrated that the mouse possesses about a 10-fold greater metabolic capacity for Roquinimex than the rat. 5. The in vivo pharmacokinetics of Roquinimex demonstrated a 7-fold higher clearance in mouse than in the rat (82 ml h(-1) kg(-1) in mouse, 10.6 ml h(-1) kg(-1) in rat), which is in concordance with the in vitro findings.
Roquinimex-induced graft-versus-host reaction after autologous bone marrow transplantation
J Am Acad Dermatol 1995 Nov;33(5 Pt 1):711-7.PMID:7593767DOI:10.1016/0190-9622(95)91806-x.
Background: Roquinimex is being used for posttransplantation immunotherapy of autologous bone marrow transplantation for acute and chronic myelogenous leukemia. This immunotherapeutic agent is a cytokine inducer and may induce an autologous graft-versus-host (GVH) and graft-versus-tumor reactions. Objective: Our purpose was to examine patients undergoing this immunotherapy for clinical signs and symptoms of acute GVH reactions and to correlate these symptoms with their clinical outcome. Methods: We studied eight patients receiving requinimex therapy. Results: We found autologous GVH reactions in three of eight patients (38%) treated with this immunotherapy. Their disease was manifested by localized or widespread violaceous papules that on histologic evaluation were compatible with a grade II GVH reaction. The acute cutaneous GVH reaction was associated with eccrine sweat gland necrosis, a dermatologic toxicity usually associated with chemotherapy. Conclusion: Long-term studies of larger numbers of patients treated with this immunotherapy will determine whether these GVH reactions confer significant, sustained, antitumor effects.
Roquinimex inhibits dextran sodium sulfate-induced murine colitis
Inflamm Res 2003 Feb;52(2):64-8.PMID:12665123DOI:10.1007/s000110300002.
Objective: Roquinimex is a modulator of the immune system and has been shown to attenuate induction of several inflammatory and autoimmune diseases. The objective of the present study was to determine the efficacy of Roquinimex in a model of murine colitis. Materials and methods: For this purpose, Balb/c mice were exposed to 5% dextran sodium sulfate (DSS) in the drinking water for five to six days. Roquinimex (300 mg kg(-1) day(-1)) was administered by subcutaneous (s.c.) injection 3 days prior to and throughout the treatment period with DSS. In separate experiments, 300 mg kg(-1) day(-1) of Roquinimex was given therapeutically after initiation of DSS challenge. Results: DSS provoked clinical signs of colitis, reduced crypt height (CH) and increased mucosal damage score (MDS) as analyzed by histology. In addition, challenge with DSS increased the colonic content of myeloperoxidase (MPO). Prophylactic administration of DSS-treated mice with Roquinimex significantly reduced clinical signs of colitis, MDS and the CH-reduction. Moreover, in Roquinimex treated animals, the MPO activity was significantly reduced by more than 50% compared to DSS control mice. Notably, therapeutic administration of Roquinimex in DSS-treated mice also significantly inhibited the MDS, CH-reduction and MPO activity. Conclusions: These findings suggest that Roquinimex strongly inhibits murine colitis and may provide a novel pharmacological approach to treat inflammatory bowel disease.