Recilisib (Ex-RAD)
(Synonyms: ON 01210) 目录号 : GC33130
Recilisib (Ex-RAD)是一种辐射防护剂，可以激活细胞中AKT和PI3K的活性。
Cas No.:334969-03-8
Sample solution is provided at 25 µL, 10mM.
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Recilisib (Ex-RAD) is a radiation protection agent that can activate the activities of AKT and PI3K in cells [1]. Recilisib can promote autophagy, enhance cell viability, and reduce cell apoptosis by activating the PI3K/AKT/mTOR pathway [2]. Recilisib can alter the cell cycle distribution pattern of cancer cells receiving radiotherapy and can be used for the treatment of acute radiation syndrome [3].
In vitro, treatment with Recilisib (10μM; 24h) significantly upregulated the protein expressions of p-PI3K, p-AKT, and p-p65 in Caco-2 cells, while the number of apoptotic cells increased, Bax and C-caspase3 expressions were upregulated, and Bcl-2 expression was decreased [4]. Treatment with Recilisib (50μM; 24h) reversed the autophagy induced by MG-132 in vascular smooth muscle cells (VSMCs), and reduced the expressions of autophagy-related proteins p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR [5].
In vivo, treatment with Recilisib (10mg/kg/day; 7 days; i.p.) exacerbated the damage to the integrity of the blood-brain barrier in a mouse model of anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis, reduced the expressions of ZO-1 and Claudin-5, and had no significant effect on the neurological damage of the mice [6]. Treatment with Recilisib (3, 100, 50, and 10mg/kg/day; i.p.) significantly increased the content of gallstones in a mouse model treated with LPS and aggravated the damage to the gallbladder mucosa [7].
References:
[1] Kang AD, et al. ON01210.Na (Ex-RAD) mitigates radiation damage through activation of the AKT pathway. PLoS One. 2013;8(3):e58355.
[2] Geng X, Zou Y, Li J, et al. BDNF alleviates Parkinson's disease by promoting STAT3 phosphorylation and regulating neuronal autophagy[J]. Cell and Tissue Research, 2023, 393(3): 455-470.
[3] Kamran M Z, Ranjan A, Kaur N, et al. Radioprotective agents: strategies and translational advances[J]. Medicinal research reviews, 2016, 36(3): 461-493.
[4] Niu M, Yin L, Duan T, et al. Asperosaponin VI alleviates TNBS-induced Crohn's disease-like colitis in mice by reducing intestinal epithelial cell apoptosis via inhibiting the PI3K/AKT/NF-κB signaling pathway[J]. Nan fang yi ke da xue xue bao= Journal of Southern Medical University, 2024, 44(12): 2335-2346.
[5] Shu Z, Li X, Zhang W, et al. MG-132 activates sodium palmitate-induced autophagy in human vascular smooth muscle cells and inhibits senescence via the PI3K/AKT/mTOR axis[J]. Lipids in health and disease, 2024, 23(1): 282.
[6] Gong Z, Lao D, Wu Y, et al. Inhibiting PI3K/Akt-Signaling pathway improves neurobehavior changes in anti-NMDAR encephalitis mice by ameliorating blood–brain barrier disruption and neuronal damage[J]. Cellular and Molecular Neurobiology, 2023, 43(7): 3623-3637.
[7] Yu J, Meng Z, Liu X, et al. Lipopolysaccharide in bile promotes the neutrophil extracellular Traps-Induced gallstone formation by activating the gallbladder immune barrier[J]. ImmunoTargets and Therapy, 2024: 789-803.
Recilisib (Ex-RAD)是一种辐射防护剂，可以激活细胞中AKT和PI3K的活性 [1]。Recilisib能够通过激活PI3K/AKT/mTOR通路促进自噬、提高细胞活力并减少细胞凋亡 [2]。Recilisib能够改变接受放射治疗的癌细胞的细胞周期分布模式，可用于治疗急性放射综合征 [3]。
在体外，Recilisib（10μM; 24h）处理显著上调了Caco-2细胞中p-PI3K、p-AKT及p-p65蛋白表达，同时细胞凋亡数量增加，Bax和C-caspase3表达上调，Bcl-2表达降低 [4]。Recilisib（50μM; 24h）处理逆转了MG-132诱导的血管平滑肌细胞（VSMC）自噬，降低了自噬相关蛋白p-PI3K/PI3K、p-AKT/AKT和p-mTOR/mTOR的表达 [5]。
在体内，Recilisib（10mg/kg/day; 7 days; i.p.）处理加剧了抗N-methyl-d-aspartate receptor（NMDAR）脑炎小鼠模型血脑屏障完整性的损害，降低了ZO-1和Claudin-5表达，而对小鼠神经损伤无明显影响 [6]。Recilisib（3, 100, 50和10mg/kg/day; i.p.）显著增加了LPS治疗的胆结石小鼠模型的胆结石含量并加重了胆囊黏膜损伤 [7]。
| Cell experiment [1]: | |
Cell lines | Vascular smooth muscle cells (VSMCs) |
Preparation Method | The VSMCs were cultured in serum-free medium supplemented with 10% fetal bovine serum, passaged, and utilized for experiments the following day once they reached a cell density of 90% in the culture dish. The experimental groups included: a control group - cultured in serum-free medium; a palmitate (PA) group - cultured in serum-free medium containing 40µM PA; PA + MG-132 group - cultured in serum-free medium containing 40µM PA and 40µM MG-132; a PA + MG-132 + Pictilisib group - cultured in serum-free medium containing 40µM PA and 2nM Pictilisib; and a PA + MG-132 + Recilisib group cultured in serum-free medium containing 40µM PA, 40µM MG-132, and 50µM Recilisib. After each group of cells was cultured in the modified medium for 24 hours, autophagy staining determination and protein blotting determination were carried out. |
Reaction Conditions | 50μM; 24h |
Applications | The treatment with Recilisib reduced the expression of autophagy-related proteins p-PI3K/PI3K, p-AKT/AKT and p-mTOR/mTOR. |
| Animal experiment [2]: | |
Animal models | C57BL / 6J mice (anti-NMDAR encephalitis mouse model) |
Preparation Method | The mice were subcutaneously immunized with 200μg of the polypeptide mixture, of which the mice in the control group were subcutaneously immunized with a mixture of equal volumes of CFA and phosphate-buffered saline (PBS). A booster injection was given 4 weeks after the immunization. All mice were intraperitoneally injected with 200ng pertussis toxin on the day of immunization and 48h after immunization. Animals were randomly divided into 4 groups: control group, model group, model + LY294002 group, and model + Recilisib group. Mice in the treatment group were intraperitoneally administered LY294002 (PI3K inhibitor, 8mg/kg) or Recilisib (10mg/kg) every day. The above treatments were given once a day for 7 consecutive days. All PI3K inhibitors and agonists were dissolved in dimethyl sulfoxide/saline (1:10). The same amount of sterile solvent was injected intraperitoneally into the control group and model group. The BBB permeability of mice was detected by the sodium fluorescein method. |
Dosage form | 10mg/kg/day for 7 days; i.p. |
Applications | Recilisib exacerbated the damage to the blood-brain barrier integrity in the mouse model of anti-NMDAR encephalitis. |
References: | |
| Cas No. | 334969-03-8 | SDF | |
| 别名 | ON 01210 | ||
| Canonical SMILES | O=C(O)C1=CC=C(/C=C/S(=O)(CC2=CC=C(Cl)C=C2)=O)C=C1 | ||
| 分子式 | C16H13ClO4S | 分子量 | 336.79 |
| 溶解度 | DMSO: 35.71 mg/mL (106.03 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。 |
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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 | 2.9692 mL | 14.846 mL | 29.6921 mL |
| 5 mM | 593.8 μL | 2.9692 mL | 5.9384 mL |
| 10 mM | 296.9 μL | 1.4846 mL | 2.9692 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 |
| 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.
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