CORM 2
(Synonyms: 三羰基二氯代钌二聚物,CORM-2) 目录号 : GC50347
CORM 2是一种能在生物体系中可控释放一氧化碳的CO释放分子，已被开发用作一氧化碳供体。
Cas No.:22594-69-0
Sample solution is provided at 25 µL, 10mM.
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CORM 2 is a carbon monoxide-releasing molecule that can liberate a controlled amount of CO in biological systems and has been developed as a carbon monoxide donor[1-2]. When CORM 2 is in contact with reduced deoxymyoglobin or deoxyhaemoglobin rapidly transfers ca. one CO equivalent to the protein haem, forming carboxymyoglobin (COMb) or carboxyhaemoglobin (COHb), respectively[3]. In addition, CORM 2 also exerts a protective effect against gastric mucosal injury induced by 75% ethanol[4].
In vitro, after treating human umbilical vein endothelial cells (HUVECs) with 100µM CORM 2 for 0-5min, a bidirectional current can be recorded. This current is insensitive to the small-, intermediate-, and large-conductance Ca2+-activated K+ channel blockers apamin (the small-conductance Ca2+-activated K+ channel blocker), TRAM-34 (the intermediate-conductance Ca2+-activated K+ channel blocker), and iberiotoxin (the big-conductance Ca2+-activated K+ channel blocker), and it is not affected by EGTA in the pipette solution[2]. RAW264.7 murine macrophage cell line was exposed to P. intermedia lipopolysaccharide (LPS) (10μg/mL) together with escalating concentrations of CORM 2 (12.5, 25, 50, 100μM) for 24h (NO) or 48h (IL-1β), and the release of both NO and IL-1β was markedly and dose-dependently suppressed[5].
In vivo, intravenous infusion of CORM 2 at 10mg/kg/h for 30min (total 5mg/kg) after cardiac arrest significantly increased neurological deficit scores (NDS), reduced S-100B levels, and improved 3-day survival in resuscitated Sprague-Dawley rats[6]. Administering CORM 2 (30mg/kg; i.p.) before a lethal dose of LPS significantly attenuated the severe hypothermia induced by LPS in C57BL/6 mice[7].
References:
[1] Khir NAM, Noh ASM, Long I, et al. Recent progress on anti-nociceptive effects of carbon monoxide releasing molecule-2 (CORM-2). Mol Cell Biochem. 2024;479(3):539-552.
[2] Dong DL, Chen C, Huang W, et al. Tricarbonyldichlororuthenium (II) dimer (CORM2) activates non-selective cation current in human endothelial cells independently of carbon monoxide releasing. Eur J Pharmacol. 2008;590(1-3):99-104.
[3] Fagone P, Mangano K, Coco M, et al. Therapeutic potential of carbon monoxide in multiple sclerosis. Clin Exp Immunol. 2012;167(2):179-187.
[4] Magierowska K, Magierowski M, Hubalewska-Mazgaj M, et al. Carbon Monoxide (CO) Released from Tricarbonyldichlororuthenium (II) Dimer (CORM-2) in Gastroprotection against Experimental Ethanol-Induced Gastric Damage. PLoS One. 2015;10(10):e0140493.
[5] Choi EY, Keum BR, Choe SH, et al. Tricarbonyldichlororuthenium(II) dimer, the lipid-soluble carbon monoxide-releasing molecule, attenuates Prevotella intermedia lipopolysaccharide-induced production of nitric oxide and interleukin-1β in murine macrophages. Int Immunopharmacol. 2021;90:107190.
[6] Wang P, Yao L, Zhou LL, et al. Carbon Monoxide Improves Neurologic Outcomes by Mitochondrial Biogenesis after Global Cerebral Ischemia Induced by Cardiac Arrest in Rats. Int J Biol Sci. 2016;12(8):1000-1009.
[7] Riquelme SA, Bueno SM, Kalergis AM. Carbon monoxide down-modulates Toll-like receptor 4/MD2 expression on innate immune cells and reduces endotoxic shock susceptibility. Immunology. 2015;144(2):321-332
CORM 2是一种能在生物体系中可控释放一氧化碳的CO释放分子，已被开发用作一氧化碳供体[1-2]。当CORM 2与还原态脱氧肌红蛋白或脱氧血红蛋白接触时，可迅速向蛋白血红素转移约1当量的CO，分别形成碳氧肌红蛋白（COMb）或碳氧血红蛋白（COHb）[3]。此外，CORM 2还对75%乙醇诱发的胃黏膜损伤具有保护作用[4]。
在体外，用100µM的CORM 2处理人脐静脉内皮细胞（HUVECs）0-5min后即可记录到双向电流。这一电流不受小电导（apamin）、中电导（TRAM-34）和大电导（iberiotoxin）钙激活钾通道阻断剂的影响，也不受电极液中EGTA的干扰[2]。RAW264.7小鼠巨噬细胞在含10µg/mL的P. intermedia脂多糖（LPS）的培养液中加入递增浓度的CORM 2（12.5、25、50、100µM），分别作用24h（测NO）或48h（测IL-1β），结果显示NO和IL-1β的释放均呈剂量依赖性显著降低[5]。
在体内，心脏骤停后给Sprague-Dawley大鼠静脉输注10mg/kg/h的CORM 2持续30min（总量5mg/kg），可显著提高神经功能缺损评分（NDS）、降低S-100B水平，并改善复苏后3天生存率[6]。在致死剂量LPS攻击前给予C57BL/6小鼠腹腔注射30mg/kg的CORM 2，可显著减轻LPS诱导的严重低体温[7]。
| Cell experiment [1]: | |
Cell lines | RAW264.7 murine macrophage cell line |
Preparation Method | Cells were incubated with the increasing dosages of CORM 2 (12.5-100μM) for 24h (measure NO) or 48h (measure IL-1β) in the presence of P. intermedia lipopolysaccharide (LPS) (10μg/ml). |
Reaction Conditions | 12.5, 25, 50, 100μM; 24h (measure NO) or 48h (measure IL-1β) |
Applications | The secretion levels of NO and IL-1β caused by P. intermedia LPS alone were obviously upregulated over those of the untreated control cells, and the administration of CORM 2 potently reduced the release of these proinflammatory mediators, and the suppressive influence was elevated with the increase of doses. CORM 2 reduced the synthesis of NO and IL-1β by approximately 83% and 84%, respectively, at the concentration of 100μM. |
| Animal experiment [2]: | |
Animal models | Male Sprague-Dawley rats |
Preparation Method | Cardiac arrest was induced by asphyxia. After 6min of untreated arrest, cardiopulmonary resuscitation (CPR) was initiated. Return of spontaneous circulation (ROSC) was defined as the restoration of a supraventricular rhythm with a mean arterial pressure (MAP)≥60mmHg sustained for at least 5min. After successful resuscitation, animals were randomly assigned to three groups: (1) CPR group—cardiac arrest was induced and CPR performed; (2) CPR+CO group—cardiac arrest was induced and CPR performed, followed by treatment with CORM 2; (3) Control group—identical surgical procedures were carried out, but cardiac arrest was not induced and CPR was omitted. Thirty minutes after ROSC, rats in the CPR+CO group received a continuous intravenous infusion of CORM 2 at 10mg/kg/h for 30min (total dose 5mg/kg). Concurrently, rats in the control and CPR groups received an equal volume of placebo (0.9% NaCl solution containing DMSO) at an infusion rate of 4mL/kg/h. |
Dosage form | 5mg/kg; intravenous infusion |
Applications | The CORM 2 treatment results showed that CO increased Neurologic deficit scores (NDS) and decreased S-100B levels significantly at 24h after ROSC. CO treatment significantly increased the 3-day survival rates of the rats after ROSC. |
References: | |
| Cas No. | 22594-69-0 | SDF | |
| 别名 | 三羰基二氯代钌二聚物,CORM-2 | ||
| Canonical SMILES | [Cl-][Ru++]1([Cl-][Ru++]([Cl-])([Cl-]1)(C#[O])(C#[O])C#[O])(C#[O])(C#[O])C#[O] | ||
| 分子式 | C6Cl4O6Ru2 | 分子量 | 512.01 |
| 溶解度 | DMSO : 30 mg/mL (58.59 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble) | 储存条件 | 4°C, away from moisture and light |
| 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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.9531 mL | 9.7654 mL | 19.5309 mL |
| 5 mM | 0.3906 mL | 1.9531 mL | 3.9062 mL |
| 10 mM | 0.1953 mL | 0.9765 mL | 1.9531 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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