规格 | 价格 | 库存 | 数量 |
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10 mM * 1 mL in DMSO |
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1mg |
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5mg |
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10mg |
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25mg |
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50mg |
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100mg |
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250mg |
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Other Sizes |
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靶点 |
XIAP (Kd = 45 nM); cIAP1 (Kd <1 nM)
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体外研究 (In Vitro) |
Birinapant 与 cIAP1 和 XIAP 结合,Kd 值分别为 45 和 1 nM。 Birinapant 显着增加 SUM149(三阴性、EGFR 激活)细胞中 TNF-α 诱导的细胞凋亡的效力,这些细胞是 TRAIL 敏感但 TRAIL 不敏感的 SUM190(ErbB2 过表达)细胞。 cIAP1 的快速降解、半胱天冬酶的激活、PARP 的裂解和 NF-B 的激活都是由 birinapant 引起的。 [1]在体外,birinapant 和 TNF-α 表现出有效的抗黑色素瘤作用。虽然这两种物质单独使用均无效,但 birinapant 与 TNF-(1 ng/mL) 联用可抑制人黑色素瘤细胞系 WTH202、WM793B、WM1366 和 WM164 的生长,IC50 分别为 1.8、2.5、7.9 和 9 nM。 birinapant 单独抑制 WM9 细胞的增殖,IC50 为 2.4 nM。在这些细胞系中,birinapant 显着抑制靶蛋白 cIAP1 和 cIAP2。 [2]
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体内研究 (In Vivo) |
Birinapant (30 mg/kg) 治疗可显着诱导黑色素瘤异种移植模型 451Lu 中肿瘤生长的消除。 [2]
在黑色素瘤异种移植模型中,Birinapant作为单一药物[2] 抑制肿瘤生长 为了研究birinapant是否能在体内作为单一药物抑制黑色素瘤肿瘤生长,我们选择了两种细胞系进行异种移植实验:两种细胞系在体外都对birinapant单一药物耐药,但451Lu在体外对birinapant与TNF-α联合治疗有反应,而1205Lu在体外对联合治疗无反应。将这两种细胞系接种于裸鼠体内,形成可触及的肿瘤,然后随机分为对照和双抗治疗组。在给药的三周内,birinapant在两种模型中都显示出抗肿瘤作用,尽管在体外联合敏感细胞系中,随着birinapant治疗动物的肿瘤生长消失,这种作用更加持久。相比之下,1205Lu肿瘤显示肿瘤生长明显减缓,但没有肿瘤消失(图5A)。 在随后的体内实验中,我们通过肿瘤裂解物的免疫印迹进一步证实了两种模型中双抗靶向抑制作用。动物再次接种异种移植模型和肿瘤。然后动物在48小时的间隔内进行两次预处理,并在第二次给药后3、6、12和24小时切除肿瘤。与对照相比,cIAP1蛋白在3h后降低到低水平,这种效果在两种模型中都持续了24小时(图5B)。在同一肿瘤的活组织检查中,活化的caspase-3染色显示,在治疗24小时后,与对照相比,biinapant处理的动物中凋亡细胞适度增加(图5C)。 药物治疗增加了ICMT-11的平均[(18)F]肿瘤摄取,CPA在24小时达到峰值(40 mg/kg;AUC40-60:基线和24小时分别为8.04±1.33和16.05±3.35 %ID/mL × min)和6小时birinapant (15 mg/kg;AUC40-60: 20.29±0.82和31.07±5.66% ID/mL × min,基线和6小时分别)。基于体素的肿瘤内在异质性时空分析表明,通过ICMT-11可以检测到离散的caspase-3激活口袋[(18)F]。肿瘤[(18)F]ICMT-11摄取增加与体外测量的caspase-3激活有关,早期放射性示踪剂摄取预测细胞凋亡,与[(18)F]氟脱氧葡萄糖- pet的糖代谢不同,后者描述细胞活力的持续丧失。 结论:CPA和birinapant的促凋亡作用导致PET检测的ICMT-11摄取呈时间依赖性增加[(18)F]。[18] [F]ICMT-11-PET有望作为caspase-3相关肿瘤细胞凋亡的无创药效学标志物。][3] |
酶活实验 |
使用荧光底物来确定物质与 XIAP 和 cIAP1 的结合亲和力,然后报告 Kd 值。首先通过用固定浓度滴定不同的蛋白质浓度(半对数稀释中的 0.075–5 μM)来计算荧光标记的修饰 Smac 肽(AbuRPF-K(5-Fam)-NH2;FP 肽)解离常数 (Kd)肽(5 nM)。测定中使用 5 nM FP 肽和 50 nM XIAP,使用 GraphPad Prism 将非线性最小二乘法拟合到单位点结合模型,生成剂量反应曲线。将 FP 肽:蛋白质二元复合物与不同浓度的 Smac 模拟物(半对数稀释液中的 100-0.001 μM)在 100 mL 0.1 M 磷酸钾缓冲液(pH 7.5,含有 100 mg/mL 牛)中混合 15 分钟。 c-球蛋白。孵育后,使用多标签读板机上的 520 nm 发射滤光片和 485 nm 激发滤光片确定偏振值。
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细胞实验 |
细胞贴壁24小时后,将细胞与birinapant和/或TNF-α一起孵育另外24或72小时。然后进行 MTS 测定。
细胞活力[1] 台盼蓝排除试验如前所述[2]。细胞接种于6孔板,每孔7.5 × 104 (SUM149)或1.5 × 105 (SUM190)细胞,粘附过夜。细胞分别用TRAIL (0-100 ng mL−1)、Birinapant (0-10,000 nM)、GT13402 (0-10,000 nM)、TNF-α (50 ng mL−1)、TNF-α中和抗体(10 μg mL−1)、pan-caspase抑制剂Q-VD-OPh (20 μM)或根据指示组合处理。所有处理均作用24 h,然后胰蛋白酶化细胞并在PBS中重悬。将10 μL细胞悬液加入10 μL 0.4%台锥蓝中,将10 μL细胞悬液载于血细胞计上;计数细胞数,记录活细胞数和死细胞数。 克隆生长试验[1] 细胞以每孔250-500个细胞(SUM149)或每孔500 - 1000个细胞(SUM190)的方式在6孔板中一式三次镀,并粘附过夜。细胞分别用TRAIL (0-100 ng mL−1)、Birinapant (0-10,000 nM)、GT13402 (0-10,000 nM)、TNF-α (50 ng mL−1)、TNF-α中和抗体(10 μg mL−1)、pan-caspase抑制剂Q-VD-OPh (20 μM)或根据指示组合处理。处理24 h后,用PBS洗涤细胞2次,加入常规培养基。然后让细胞生长5-14天,每4-5天更换一次培养基。一旦观察到至少50个细胞的菌落,用PBS洗涤,固定,用0.4%结晶紫染色,然后用冷水冲洗并放置干燥过夜。使用ColCount对菌落进行计数和成像,并计算每个镀细胞形成的菌落。数值归一化为未治疗。 Annexin-V染色[1] 细胞接种于6孔板,每孔7.5 × 104 (SUM149)或1.5 × 105 (SUM190)细胞,粘附过夜。将细胞用TRAIL (0-100 ng mL−1)、Birinapant (0 - 1000 nM)、GT13402 (0 - 1000 nM)或组合处理12小时。用0.25%胰蛋白酶(-EDTA)收获细胞,用PBS洗涤,在生物素偶联的Annexin-V中重悬5分钟。再用PBS洗涤细胞,用链霉亲和素偶联的FITC和7-AAD染料在冰上重悬15分钟。细胞在PBS中洗涤并重悬,然后在BD FACSCalibur流式细胞仪上收集至少25,000个事件。采用FlowJo软件对结果进行分析。 TNFR1敲低[1] 细胞接种于6孔板中,每孔1.5 × 105个细胞,粘附过夜。24 h后,在dharmect转染试剂的存在下,使用100 nM的scramble control siRNA或靶向TNFR1 siRNA。转染后第1天加入Birinapant(0-1,000 nM), 24 h后收获细胞进行台盼蓝活力染色和western免疫印迹,确认敲除。 体外药敏试验[2] 对于单层细胞培养实验,细胞被允许附着24小时,随后与Birinapant和/或TNF-α孵育24或72小时。CellTiter 96®水相非放射性细胞增殖试验(MTS)根据制造商的说明进行。为了进行细胞周期分析,将黑色素瘤细胞固定在70%乙醇中,并用碘化丙啶染色。随后用EPICS XL仪器分析样品。根据制造商的描述,用膜联蛋白V异藻蓝蛋白偶联物进行膜联蛋白V染色。简单地说,用DMSO对照、Birinapant和/或TNF-α处理细胞24小时。将重悬的细胞洗净,用偶联物孵育15min,加入膜联蛋白结合缓冲液。随后用EPICS XL仪器分析样品。 451Lu和WM1366黑色素瘤细胞用Birinapant1uM联合TNF-α 1ng/ml治疗。然后将细胞在存在或不存在Z-VAD-FMK(泛caspase抑制剂)的情况下孵育72小时。使用MTS法评估增殖。 451Lu和WM1366黑色素瘤细胞用Birinapant 1uM联合TNF-α 1ng/ml治疗。然后将细胞在存在或不存在Necrostatin-1 (RIP1激酶抑制剂)的情况下孵育72小时。使用MTS法评估增殖。[2] |
动物实验 |
Human melanoma xenografts 451Lu
30 mg/kg 3 times per week intraperitoneally All animal experiments were performed in accordance with Wistar IACUC protocol 111954 in NUDE mice. Ten animals each were inoculated s.c. with 1×106 451Lu or 1205Lu human melanoma cells in a suspension of matrigel / complete media at a ratio of 1:1. After formation of palpable tumors, mice from both tumor models were randomized into two groups. Both groups were treated intra-peritoneal three times/ week with either vehicle control or Birinapant 30mg/kg for 21 days. Birinapant was dissolved in 12.5% Captisol in distilled water. Tumor size was assessed twice weekly by caliper measurement. Subsequently, satellite groups of ten and fifteen mice were inoculated in the same fashion with 451Lu and 1205Lu tumor cells respectively. After tumors had reached a mean volume of 200mm3 animals were dosed with either Birinapant or vehicle control as described above. After 48 hours and two doses, animals were sacrificed and tumors were harvested at four time points after the last treatment. Tumor samples were snap frozen in liquid nitrogen for subsequent protein analysis and preserved as FFPE blocks for immune-histochemistry. [2] Small animal experimental models [3] The in vivo experimental xenograft models were established by subcutaneous injection of 5 × 103 38C13 cells in C3H mice and 5 × 106 HCT116 or 2 × 106 MDA-MB-231 cells in BALB/c nude mice. All mice were 6- to 8-week-old females from Charles River. When xenografts reached approximately 80 mm3 [tumor dimensions were measured using a caliper and tumor volumes were calculated using the ellipsoid formula that is best for estimating tumor mass; volume mm3 = (π/6) × a × b × c, where a, b, and c represent 3 orthogonal axes of the tumor], mice were injected a single dose of CPA (40 mg/kg i.p.) or Birinapant (15 m/kg i.p.) and subjected to positron emission tomography-computed tomography (PET-CT) imaging in a longitudinal setting where the same animal serves as its own control. |
参考文献 |
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其他信息 |
Birinapant is a dipeptide.
Birinapant has been investigated for the treatment of Myelodysplastic Syndrome (MDS) and Chronic Myelomonocytic Leukemia (CMML). Birinapant is a synthetic small molecule that is both a peptidomimetic of second mitochondrial-derived activator of caspases (SMAC) and inhibitor of IAP (Inhibitor of Apoptosis Protein) family proteins, with potential antineoplastic activity. As a SMAC mimetic and IAP antagonist, birinapant selectively binds to and inhibits the activity of IAPs, such as X chromosome-linked IAP (XIAP) and cellular IAPs 1 (cIAP1) and 2 (cIAP2), with a greater effect on cIAP1 than cIAP2. Since IAPs shield cancer cells from the apoptosis process, this agent may restore and promote the induction of apoptosis through apoptotic signaling pathways in cancer cells and inactivate the nuclear factor-kappa B (NF-kB)-mediated survival pathway. IAPs are overexpressed by many cancer cell types. They are able to suppress apoptosis by binding to, via their baculoviral lAP repeat (BIR) domains, and inhibiting active caspases-3, -7 and -9. IAP overexpression promotes both cancer cell survival and chemotherapy resistance. X-linked inhibitor of apoptosis protein (XIAP), the most potent mammalian caspase inhibitor, has been associated with acquired therapeutic resistance in inflammatory breast cancer (IBC), an aggressive subset of breast cancer with an extremely poor survival rate. The second mitochondria-derived activator of caspases (Smac) protein is a potent antagonist of IAP proteins and the basis for the development of Smac mimetic drugs. Here, we report for the first time that bivalent Smac mimetic Birinapant induces cell death as a single agent in TRAIL-insensitive SUM190 (ErbB2-overexpressing) cells and significantly increases potency of TRAIL-induced apoptosis in TRAIL-sensitive SUM149 (triple-negative, EGFR-activated) cells, two patient tumor-derived IBC models. Birinapant has high binding affinity (nM range) for cIAP1/2 and XIAP. Using isogenic SUM149- and SUM190-derived cells with differential XIAP expression (SUM149 wtXIAP, SUM190 shXIAP) and another bivalent Smac mimetic (GT13402) with high cIAP1/2 but low XIAP binding affinity (K (d) > 1 μM), we show that XIAP inhibition is necessary for increasing TRAIL potency. In contrast, single agent efficacy of Birinapant is due to pan-IAP antagonism. Birinapant caused rapid cIAP1 degradation, caspase activation, PARP cleavage, and NF-κB activation. A modest increase in TNF-α production was seen in SUM190 cells following Birinapant treatment, but no increase occurred in SUM149 cells. Exogenous TNF-α addition did not increase Birinapant efficacy. Neutralizing antibodies against TNF-α or TNFR1 knockdown did not reverse cell death. However, pan-caspase inhibitor Q-VD-OPh reversed Birinapant-mediated cell death. In addition, Birinapant in combination or as a single agent decreased colony formation and anchorage-independent growth potential of IBC cells. By demonstrating that Birinapant primes cancer cells for death in an IAP-dependent manner, these findings support the development of Smac mimetics for IBC treatment. [1] Purpose: Inhibitor of apoptosis proteins (IAP) promote cancer cell survival and confer resistance to therapy. We report on the ability of second mitochondria-derived activator of caspases mimetic, birinapant, which acts as antagonist to cIAP1 and cIAP2, to restore the sensitivity to apoptotic stimuli such as TNF-α in melanomas. Experimental design: Seventeen melanoma cell lines, representing five major genetic subgroups of cutaneous melanoma, were treated with birinapant as a single agent or in combination with TNF-α. Effects on cell viability, target inhibition, and initiation of apoptosis were assessed and findings were validated in 2-dimensional (2D), 3D spheroid, and in vivo xenograft models. Results: When birinapant was combined with TNF-α, strong combination activity, that is, neither compound was effective individually but the combination was highly effective, was observed in 12 of 18 cell lines. This response was conserved in spheroid models, whereas in vivo birinapant inhibited tumor growth without adding TNF-α in in vitro resistant cell lines. Birinapant combined with TNF-α inhibited the growth of a melanoma cell line with acquired resistance to BRAF inhibition to the same extent as in the parental cell line. Conclusions: Birinapant in combination with TNF-α exhibits a strong antimelanoma effect in vitro. Birinapant as a single agent shows in vivo antitumor activity, even if cells are resistant to single agent therapy in vitro. Birinapant in combination with TNF-α is effective in a melanoma cell line with acquired resistance to BRAF inhibitors. [2] Purpose: Induction of apoptosis in tumors is considered a desired goal of anticancer therapy. We investigated whether the dynamic temporal and spatial evolution of apoptosis in response to cytotoxic and mechanism-based therapeutics could be detected noninvasively by the caspase-3 radiotracer [(18)F]ICMT-11 and positron emission tomography (PET). Experimental design: The effects of a single dose of the alkylating agent cyclophosphamide (CPA or 4-hydroperoxycyclophosphamide), or the mechanism-based small molecule SMAC mimetic birinapant on caspase-3 activation was assessed in vitro and by [(18)F]ICMT-11-PET in mice bearing 38C13 B-cell lymphoma, HCT116 colon carcinoma, or MDA-MB-231 breast adenocarcinoma tumors. Ex vivo analysis of caspase-3 was compared to the in vivo PET imaging data. [3] The acquisition of apoptosis resistance is a fundamental event in cancer development. Among the mechanisms used by cancer cells to evade apoptosis is the dysregulation of inhibitor of apoptosis (IAP) proteins. The activity of the IAPs is regulated by endogenous IAP antagonists such as SMAC (also termed DIABLO). Antagonism of IAP proteins by SMAC occurs via binding of the N-terminal tetrapeptide (AVPI) of SMAC to selected BIR domains of the IAPs. Small molecule compounds that mimic the AVPI motif of SMAC have been designed to overcome IAP-mediated apoptosis resistance of cancer cells. Here, we report the preclinical characterization of birinapant (TL32711), a bivalent SMAC-mimetic compound currently in clinical trials for the treatment of cancer. Birinapant bound to the BIR3 domains of cIAP1, cIAP2, XIAP, and the BIR domain of ML-IAP in vitro and induced the autoubiquitylation and proteasomal degradation of cIAP1 and cIAP2 in intact cells, which resulted in formation of a RIPK1:caspase-8 complex, caspase-8 activation, and induction of tumor cell death. Birinapant preferentially targeted the TRAF2-associated cIAP1 and cIAP2 with subsequent inhibition of TNF-induced NF-κB activation. The activity of a variety of chemotherapeutic cancer drugs was potentiated by birinapant both in a TNF-dependent or TNF-independent manner. Tumor growth in multiple primary patient-derived xenotransplant models was inhibited by birinapant at well-tolerated doses. These results support the therapeutic combination of birinapant with multiple chemotherapies, in particular, those therapies that can induce TNF secretion.[4] |
分子式 |
C42H56F2N8O6
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分子量 |
806.94
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精确质量 |
806.42909
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元素分析 |
C, 62.51; H, 6.99; F, 4.71; N, 13.89; O, 11.90
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CAS号 |
1260251-31-7
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相关CAS号 |
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PubChem CID |
49836020
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外观&性状 |
White solid powder
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密度 |
1.3±0.1 g/cm3
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沸点 |
1090.5±65.0 °C at 760 mmHg
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闪点 |
613.3±34.3 °C
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蒸汽压 |
0.0±0.3 mmHg at 25°C
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折射率 |
1.628
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LogP |
2.98
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tPSA |
174.1
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氢键供体(HBD)数目 |
8
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氢键受体(HBA)数目 |
10
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可旋转键数目(RBC) |
15
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重原子数目 |
58
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分子复杂度/Complexity |
1350
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定义原子立体中心数目 |
8
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SMILES |
FC1C([H])=C([H])C2=C(C=1[H])N([H])C(C1=C(C3C([H])=C([H])C(=C([H])C=3N1[H])F)C([H])([H])[C@]1([H])C([H])([H])[C@@]([H])(C([H])([H])N1C([C@]([H])(C([H])([H])C([H])([H])[H])N([H])C([C@]([H])(C([H])([H])[H])N([H])C([H])([H])[H])=O)=O)O[H])=C2C([H])([H])[C@]1([H])C([H])([H])[C@@]([H])(C([H])([H])N1C([C@]([H])(C([H])([H])C([H])([H])[H])N([H])C([C@]([H])(C([H])([H])[H])N([H])C([H])([H])[H])=O)=O)O[H]
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InChi Key |
PKWRMUKBEYJEIX-DXXQBUJASA-N
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InChi Code |
InChI=1S/C42H56F2N8O6/c1-7-33(49-39(55)21(3)45-5)41(57)51-19-27(53)15-25(51)17-31-29-11-9-23(43)13-35(29)47-37(31)38-32(30-12-10-24(44)14-36(30)48-38)18-26-16-28(54)20-52(26)42(58)34(8-2)50-40(56)22(4)46-6/h9-14,21-22,25-28,33-34,45-48,53-54H,7-8,15-20H2,1-6H3,(H,49,55)(H,50,56)/t21-,22-,25-,26-,27-,28-,33-,34-/m0/s1
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化学名 |
(2S)-N-[(2S)-1-[(2R,4S)-2-[[6-fluoro-2-[6-fluoro-3-[[(2R,4S)-4-hydroxy-1-[(2S)-2-[[(2S)-2-(methylamino)propanoyl]amino]butanoyl]pyrrolidin-2-yl]methyl]-1H-indol-2-yl]-1H-indol-3-yl]methyl]-4-hydroxypyrrolidin-1-yl]-1-oxobutan-2-yl]-2-(methylamino)propanamide
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别名 |
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HS Tariff Code |
2934.99.9001
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存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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溶解度 (体外实验) |
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溶解度 (体内实验) |
配方 1 中的溶解度: ≥ 2.08 mg/mL (2.58 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。
例如,若需制备1 mL的工作液,可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中,混匀;然后向上述溶液中加入50 μL Tween-80,混匀;加入450 μL生理盐水定容至1 mL。 *生理盐水的制备:将 0.9 g 氯化钠溶解在 100 mL ddH₂O中,得到澄清溶液。 配方 2 中的溶解度: 2.08 mg/mL (2.58 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加,逐一添加), 悬浊液; 超声助溶。 例如,若需制备1 mL的工作液,可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中,混匀。 *20% SBE-β-CD 生理盐水溶液的制备(4°C,1 周):将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中,得到澄清溶液。 View More
配方 3 中的溶解度: ≥ 2.08 mg/mL (2.58 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。 配方 4 中的溶解度: 15% Captisol: 15mg/mL 1、请先配制澄清的储备液(如:用DMSO配置50 或 100 mg/mL母液(储备液)); 2、取适量母液,按从左到右的顺序依次添加助溶剂,澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明,并不一定代表此产品 的实际溶解配方): 10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline); 假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀/澄清;向上述体系中加入50 μL Tween-80,混合均匀/澄清;然后继续加入450 μL ddH2O (或 saline)定容至 1 mL; 3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例; 4、 如产品在配制过程中出现沉淀/析出,可通过加热(≤50℃)或超声的方式助溶; 5、为保证最佳实验结果,工作液请现配现用! 6、如不确定怎么将母液配置成体内动物实验的工作液,请查看说明书或联系我们; 7、 以上所有助溶剂都可在 Invivochem.cn网站购买。 |
制备储备液 | 1 mg | 5 mg | 10 mg | |
1 mM | 1.2392 mL | 6.1962 mL | 12.3925 mL | |
5 mM | 0.2478 mL | 1.2392 mL | 2.4785 mL | |
10 mM | 0.1239 mL | 0.6196 mL | 1.2392 mL |
1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;
3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);
4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。
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)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。
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 ddH2O,混匀澄清。
(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
(2) 一定要按顺序加入溶剂 (助溶剂) 。
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