Cridanimod (sodium salt)
(Synonyms: 吖啶酮乙酸钠) 目录号 : GC45413
An inducer of type I interferon production
Cas No.:58880-43-6
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
Cridanimod is an inducer of type I interferon (IFN) production.1,2 It induces IRF3 phosphorylation, IFN-β production, and NF-κB activation in wild-type, but not in stimulator of interferon genes (STING) mutant, murine macrophages.1 In vivo, cridanimod (112-1,792 mg/kg) increases plasma levels of IFN in weanling and adult mice.2 Cridanimod inhibits viral infection in mouse models of Semliki forest, coxsackie B1, Columbia SK, herpes, and pseudorabies viruses with protective doses (PD50s) ranging from 17-320 mg/kg.3 It increases uterine expression of estrogen and progesterone receptors in ovariectomized rats.4 Cridanimod also reverses tamoxifen-induced decreases in progesterone receptor expression in young rats.
References
1. Cavlar, T., Deimling, T., Ablasser, A., et al. Species-specific detection of the antiviral small-molecule compound CMA by STING. EMBO J. 32(10), 1440-1450 (2013).
2. Taylor, J.L., Schoenherr, C.K., and Grossberg, S.E. High-yield interferon induction by 10-carboxymethyl-9-acridanone in mice and hamsters. Antimicrob. Agents Chemother. 18(1), 20-26 (1980).
3. Kramer, M.J., Cleeland, R., and Grunberg, E. Antiviral activity of 10-carboxymethyl-9-acridanone. Antimicrob. Agents Chemother. 9(2), 233-238 (1976).
4. Surkov, K.G., Tsyrlina, E.V., Konstantinova, M.M., et al. Neovir, an interferon inductor, modifies expression of steroid hormone receptors in hormone-dependent tissues and restores sensitivity to tamoxifen in patients with inoperable breast cancer. Vopr. Onkol. 42(6), 28-32 (1996).
| Cas No. | 58880-43-6 | SDF | |
| 别名 | 吖啶酮乙酸钠 | ||
| Canonical SMILES | O=C1C2=CC=CC=C2N(CC([O-])=O)C3=C1C=CC=C3.[Na+] | ||
| 分子式 | C15H10NO3.Na | 分子量 | 275.2 |
| 溶解度 | DMSO: 20 mg/ml | 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 | 3.6337 mL | 18.1686 mL | 36.3372 mL |
| 5 mM | 0.7267 mL | 3.6337 mL | 7.2674 mL |
| 10 mM | 0.3634 mL | 1.8169 mL | 3.6337 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。
Antiviral activity of 10-carboxymethyl-9-acridanone
Antimicrob Agents Chemother 1976 Feb;9(2):233-8.PMID:1267425DOI:10.1128/AAC.9.2.233.
Intraperitoneal administration of 10-carboxymethyl-9-acridanone sodium salt (CMA) protected at least 50% of mice tested from otherwise lethal infections with Semliki forest, coxsackie B1, Columbia SK, Western equine encephalitis, herpes simplex, and pseudorabies viruses. The protective effect against influenza A2/Asian/J305 and coxsackie A21 viruses was less but was statistically significant. When administered either subcutaneously or orally, CMA protected at least 50% of mice against Semliki forest and pseudorabies viruses; the effect against coxsackie B1 and herpes simplex viruses was less but was statistically significant. Initiation of treatment could be delayed from 2 to 24 h after infection of mice with coxsackie B1, herpes simplex, Semliki forest, and Western equine encephalitis viruses without loss of an antiviral effect. CMA did not inactivate Semliki forest or coxsackie B1 viruses on contact and was without effect against any of the viruses tested in tissue culture by the tube dilution assay. The humoral antibody response in mice to both influenza virus and sheep erythrocytes was unaffected by CMA. After administration of CMA, an interferon-like substance was induced in mice or mouse cell culture but not in rabbits or rabbit cell culture.
Interaction of sodium salt of 9-oxo-10-acridineacetic acid (CMA) and its analogs with serum albumin. A model for study on binding of the interferon inducer with receptor
Arch Immunol Ther Exp (Warsz) 1985;33(2):299-310.PMID:2417573doi
Equilibrium dialysis, gel filtration and SDS polyacrylamide gel electrophoresis were used to study the interaction of sodium salt of 9-oxo-10-acridineacetic acid (CMA) as well as its analogs 7, 8, 11, 13 - 16 with proteins. The compounds were found to bind mainly to serum albumins. Several other proteins had no affinity to the compounds. The close analogs 7 and 8 (sodium salt of 2,7-dibromo-9-oxo-10-acridineacetic acid and sodium salt of 9-oxo-10-acridinebutyric acid) which were inactive as interferon inducers were found to have greater affinity to bovine, mouse or human albumin than the active IFN inducer--CMA. The mechanism of interaction of CMA as well as its close analogs with albumin resembled the first phase of reaction of pharmacologically active ligands with their specific receptor or acceptor proteins. CMA and some of its close analogs were also shown to stabilize the human erythrocyte membrane against hemolysis in the hypotonic solution. However, the activity of the compounds was much weaker than that of other so called membrane active drugs.
Tolerance or hyperreactivity to interferon induction by sodium salt of 9-oxo-10-acridineacetic acid and analogs in mice and in the mouse macrophage cultures
Arch Immunol Ther Exp (Warsz) 1987;35(3):389-95.PMID:3446087doi
Choline and halogen analogs of 9-oxo-10-acridineacetic acid (CMA) were studied as IFN inducers in mice and in the mouse bone marrow-derived macrophage cultures. Two of the choline analogs--DMCMA and CSCMA were inducers of IFN in the macrophages. The response was found to be dose related. CMA as well as the active analogs were found to induce the hyporeactive state to IFN induction both in mice and in the mouse macrophage cultures. On the other hand, the inhibitor of IFN induction by CMA--the dibromo analog (DBCMA) was found to induce in mice a hyperreactive state to IFN induction by CMA.
Competition of sodium salt of 9-oxo-10-acridineacetic acid with analogs during induction of interferon in the mouse bone marrow-derived macrophages
Arch Immunol Ther Exp (Warsz) 1985;33(2):287-97.PMID:3878695doi
Analogs of 9-oxo-10-acridineacetic acid (CMA) including new synthetic compounds, were found to be valuable tools for investigating the mechanism of interferon (IFN) induction. Experiments were performed on the long-term cultures of mouse bone marrow-derived macrophages which are unusually susceptible to IFN induction by CMA. CMA in the optimal nontoxic concentration of 600 micrograms/ml may induce in the macrophages up to 3.500 units of IFN/ml. The response was found to be dose related. The analogs of CMA, compounds 3, 7-16, were found to be inactive as IFN inducers. However, the analogs 3, and 8-16 administered together with the suboptimal doses of CMA enhanced by 10 to 40-fold the interferon response to CMA. On the other hand, the compound 7 was shown to inhibit completely the induction of interferon by CMA. L-tryptophan was inactive as either enhancer or inhibitor of CMA. The mode of action of CMA is explained in terms of the hormonal concept of IFN induction.
Induction of interferon in mice by sodium salt of 9-oxo-10-acridineacetic acid: specific enhancement by analogs
Arch Immunol Ther Exp (Warsz) 1985;33(2):275-85.PMID:2417572doi
9-oxo-10-acridineacetic acid bearing the common name of 10-carboxymethyl-9-acridanone or CMA (6) was found to be a very potent interferon (IFN) inducer in adult Balb/c mice. Seven structural analogs of CMA were synthetized and assayed for the interferon inducing ability. Three of the compounds had new chemical structures. The analogs were shown to be either weak or inactive interferon inducers. However, some of the analogs administered intraperitoneally (i.p.) or orally (p.o.) either 2 h before CMA or together with the active inducer enhanced by 10 to 60-fold the serum interferon response. We suggest that CMA induces interferon indirectly via a specific protein receptor. The specific enhancement of the serum interferon response to CMA by its inactive analogs may be explained in terms of the competition of the compounds for binding sites at the acceptor or transporting protein molecules. In the presence of an analog of CMA greater amount of free CMA may be available for the receptors in the target cells than when CMA acts alone. Only CMA bound to the receptor would be biologically active whereas the complexes of the compounds with the acceptor are biologically inert.