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My CartCAS：459868-92-9
Storage：Powder:2-8℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year
Purity：≥98%
Appearance：Light yellow to yellow Solid
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| CAS | 459868-92-9 |
| Name | Rucaparib phosphate |
| Molecular Formula | C19H18FN3O·H3PO4 |
| Molecular Weight | 421.36 |
| Solubility | Soluble in DMSO ≥3mg/mL |
| Purity | ≥98% |
| Appearance | Light yellow to yellow Solid |
| Storage | Powder:2-8℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year |
| MDL | MFCD17010269 |
| SMILES | O=P(O)(O)O.FC1=CC2=C3C(CCNC2=O)=C(C4=CC=C(CNC)C=C4)NC3=C1 |
| Target Point | PARP |
| Passage | Cell Cycle;DNA Damage/DNA Repair; Epigenetics |
| Background | It is a potent PARP1/2/3 inhibitor. |
| Biological Activity | Rucaparib (AG-014699, PF-01367338)是有效可口服的 PARP1/2/3 抑制剂，结合PARP1的Ki为1.4 nM，对PARP其余亚型也有亲和性。[1-4] |
| In Vitro | 在透化的D283Med细胞中，Rucaparib在浓度为1μM时抑制PARP-1活性97.1％[3]。Rucaparib是酶测定中最有效的PARP抑制剂(Ki，1.4 nM)，以及AG14644可能的N-去甲基化代谢物[1]。 Rucaparib的放射增敏是由于NF-κB活化的下游抑制，并且与SSB修复抑制无关。 Rucaparib可以靶向由DNA损伤激活的NF-κB，并克服经典NF-κB抑制剂观察到的毒性，而不会损害其他重要的炎症功能[2]。 |
| In Vivo | Rucaparib和AG14584显著(P <0.05)增加替莫唑胺的毒性。 Rucaparib(1 mg / kg)显著增加替莫唑胺引起的体重减轻。 Rucaparib(0.1 mg / kg)导致替莫唑胺诱导的肿瘤生长延迟增加50％[1]。 Rucaparib无毒，但在DNA修复蛋白质感受力的D384Med异种移植物中显著增强替莫唑胺诱导的TGD。药代动力学研究还表明Rucaparib在脑组织中被检测到，这表明Rucaparib在颅内恶性肿瘤治疗中具有潜力[3]。 Rucaparib显著增强拓扑替康和替莫唑胺在NB-1691，SH-SY-5Y和SKNBE(2c)细胞中的细胞毒性。 Rucaparib增强替莫唑胺的抗肿瘤活性，并表明NB1691和SHSY5Y异种移植物完全和持续的肿瘤消退[4]。 |
| Cell Experiment | 成神经管细胞瘤细胞系分别以1×103，3×103和3×103的密度接种在96孔板中。在接种后24小时(D384Med)或48小时(D283Med和D425Med)，在存在或不存在0.4μMRucaparib的情况下将细胞暴露于各种浓度的替莫唑胺。在培养3天(D425Med和D384Med)或5天(D283Med)后，通过XTT细胞增殖试剂盒测定评估细胞活力。细胞生长表示为相对于DMSO或0.4μMRucaparib单独对照的百分比。计算单独或与Rucaparib组合的替莫唑胺的浓度，其抑制生长50％(GI50)。增强因子50(PF50)定义为在Rucaparib存在下替莫唑胺的GI50与单独的替莫唑胺的GI50的比率。 |
| Animal Experiment | 单剂量的替莫唑胺以200mg/kg的盐水悬浮液单独给药或与单次ip给药的PARP抑制剂联合给药，剂量为0.1 [Rucaparib和MS-AG14644(仅相当于0.078mg/kg游离AG14644))，1.0和10mg/kg(对于甲磺酸盐，相当于0.79和7.9mg/kg游离AG14451和AG14452和0.78和7.8游离AG14531和AG14644)。对照动物用生理盐水po和ip或生理盐水po和PARP抑制剂10mg/kg ip处理 |
| Kinase Experiment | 与仅DMSO相比，使用各种浓度的Rucaparib(0-1μM)测量5×103D28383Med细胞中PARP活性的抑制。通过免疫学在透化细胞的样品中测量最大刺激的PARP活性。 |
| Data Literature Source | [1]. Thomas HD，et al. Preclinical selection of a novel poly(ADP-ribose) polymerase inhibitor for clinical trial. Mol Cancer Ther，2007，6(3)，945-956. [2]. Hunter JE，et al. NF-κB mediates radio-sensitization by the PARP-1 inhibitor，AG-014699. Oncogene，2012，31(2)，251-264. [3]. Daniel RA，et al. Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699. Br J Cancer，2010，103(10)，1588-1596. [4]. Daniel RA，et al. Inhibition of poly(ADP-ribose) polymerase-1 enhances temozolomide and topotecan activity against childhood neuroblastoma. Clin Cancer Res，2009，15(4)，1241-1249. |
| Unit | Bottle |
| Specification | 5mg 10mg |
是有效的 PARP1/2/3 抑制剂。
Remark：These protocols are for reference only. Solarbio does not independently validate these methods.
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