MK-2206 HCl

别名: MK2206; MK-2206 hydrochloride; 1032349-77-1; MK-2206 Monohydrochloride; UNII-4HA45S22ZZ; 4HA45S22ZZ; 1,2,4-Triazolo(3,4-f)(1,6)naphthyridin-3(2H)-one, 8-(4-(1-aminocyclobutyl)phenyl)-9-phenyl-, hydrochloride (1:1); 8-[4-(1-aminocyclobutyl)phenyl]-9-phenyl-2H-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3-one;hydrochloride; MK2206; MK 2206 8-[4-(1-aminocyclobutyl)phenyl]-9-phenyl-2H-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3-one,hydrochloride
目录号: V39562 纯度: ≥98%
MK-2206 (MK2206) 是一种新型、有效的 Akt 抑制剂,具有抗癌活性。
MK-2206 HCl CAS号: 1032349-77-1
产品类别: New2
产品仅用于科学研究,不针对患者销售
规格 价格
500mg
1g
Other Sizes

Other Forms of MK-2206 HCl:

  • MK2206盐酸盐
  • MK2206
点击了解更多
InvivoChem产品被CNS等顶刊论文引用
产品描述
MK-2206 (MK2206) 是一种新型、有效的 Akt 抑制剂,具有抗癌活性。它抑制 AKT,Akt1、Akt2 和 Akt3 的 IC50 分别为 8、12 和 65 nM。
生物活性&实验参考方法
靶点
Akt1 (IC50 = 8 nM); Akt2 (IC50 = 12 nM); Akt3 (IC50 = 65 nM) Akt1 (IC50 = 8 nM); Akt2 (IC50 = 12 nM); Akt3 (IC50 = 65 nM)
体外研究 (In Vitro)
MK-2206(0-10 μM;72 和 96 小时)以剂量和时间依赖性方式抑制鼻咽癌 (NPC) 细胞系 CNE-1、CNE-2、HONE-1 和 SUNE 的生长-1[3]。对于 CNE-2 和 HONE-1 细胞,MK-2206(0-10 μM;24 和 48 小时)会导致 G0/G1 期细胞比例呈剂量依赖性上升,而 S 期细胞数量相应减少[3 ]。 MK-2206(0-10 μM;24 小时)以剂量依赖性方式减弱 S6 和 PRAS40 的磷酸化水平。 GSKα/β 和 AKT 磷酸化不受 MK-2206 影响。[/3]。在 CNE-2 细胞中,MK -2206(0-10 μM;24 小时)剂量依赖性地促进 LC3-II 的出现。自噬需要关键的蛋白质微管相关蛋白 1 (LC3)[3]。
体内研究 (In Vivo)
两种口服灌胃剂量(480 mg/kg 每周一次,240 mg/kg 每周 3 次;持续两周)的 MK-2206 均可抑制裸鼠中人 CNE-2 异种移植物的发育。在小鼠中,没有发现进一步明显的伤害[3]。口服给药时,MK-2206(隔天 120 mg/kg)可显着减少携带 GEO 结肠癌细胞的 3-5 周龄无胸腺裸鼠的肿瘤形成[4]。
酶活实验
Akt 激酶通过 GSK 衍生的生物素化肽底物进行检测。通过将磷酸肽特异的镧系螯合物 (Lance) 偶联单克隆抗体与链霉亲和素连接的别藻蓝蛋白 (SA-APC) 荧光团(可与肽的生物素部分结合)相结合,可以使用均相时间分辨荧光 (HTRF)以确定磷酸化程度。当喷枪和APC靠近时,喷枪将非辐射能量转移到APC,然后APC发射波长为655 nm的光。蛋白酶抑制剂混合物 (PIC) 100X:苯甲脒 1 mg/mL、胃酶抑素 0.5 mg/mL、亮肽素 0.5 mg/mL、抑肽酶 0.5 mg/mL; 10X 检测试剂:20 mM 9-甘油磷酸、50 mM HEPES、pH 7.3、16.6 mM EDTA、0.1% BSA、0.1% Triton X-100、0.17 nM 标记单克隆抗体和 0.0067 mg/mL SA-APC 组成淬灭缓冲液。 ATP/MgCl2 测定的工作溶液:1X 测定缓冲液、1 mM DTT、1X PIC、5% 甘油、活性 Akt;肽工作溶液:2 TM GSK 生物素化肽、1X 检测缓冲液、1 mM DTT、1X PIC 和 5% 甘油。通过向适当的孔中添加 16 µL ATP/MgCl2 工作溶液来组装反应。添加 MK-2206 或载体 (1.0 µL),然后添加 10 µL 肽工作溶液。加入 13 μL 酶工作液并混合开始反应。允许反应进行 50 分钟,然后通过添加 60 µL HTRF 淬灭缓冲液来停止。停止的反应在室温下孵育至少30分钟,然后在仪器中读数。
细胞实验
细胞增殖测定[3]
细胞类型: NPC 细胞系 CNE-1、CNE-2、HONE-1 和 SUNE-1
测试浓度: 0.08、0.16、0.31、0.63、1.25、2.5、5、10 μM
孵育时间:72 和 96 小时
实验结果: 72 和 96 小时时,CNE-1、CNE-2 和 HONE-1 细胞系中的 IC50 值为 3-5 μM,而在 SUNE-1 中,IC50 值小于 1 μM。

细胞周期分析[3]
细胞类型: CNE-2 和 HONE-1 细胞
测试浓度: 0.625、1.25、 2.5、5、10 μM
孵育时间:24 或 48 小时
实验结果:以剂量依赖性方式诱导细胞周期停滞在 G1方式。

蛋白质印迹分析[3]
细胞类型: SUNE-1 和 CNE-2 细胞
测试浓度: 0.625、1.25、 2.5、5、10 μM
孵育时间:24 小时
实验结果:抑制 AKT 下游靶点的磷酸化。细胞自噬测定[3]
细胞类型: CNE-2 细胞
测试浓度: 0.625、1.25、2.5、5、10 μM
孵育持续时间:24小时
实验结果:诱导自噬。
动物实验
Animal/Disease Models: Four - to 6weeks old male BALB/c nude mice with CNE-2 xenografts[3]
Doses: 240 mg/kg and 480 mg/kg
Route of Administration: po (oral gavage); 240 mg/kg for three times a week; 480 mg/ kg for once a week; for 2 weeks
Experimental Results: Both doses inhibited the growth of human CNE-2 xenografts in nude mice.
参考文献

[1]. Abstract #DDT01-1: MK-2206: A potent oral allosteric AKT inhibitor. 2009.

[2]. Phase II trial of AKT inhibitor MK-2206 in patients with advanced breast cancer who have tumors with PIK3CA or AKT mutations, and/or PTEN loss/PTEN mutation. Breast Cancer Res. 2019 Jul 5;21(1):78.

[3]. Effects of an oral allosteric AKT inhibitor (MK-2206) on human nasopharyngeal cancer in vitro and in vivo. Drug Des Devel Ther. 2014 Oct 10;8:1827-37.

[4]. Akt inhibitor MK-2206 promotes anti-tumor activity and cell death by modulation of AIF and Ezrin in colorectal cancer. BMC Cancer. 2014 Mar 1;14:145.

其他信息
The PI3K pathway plays an important role in regulating cancer cell proliferation, growth, survival and metabolism. The serine/threonine kinase Akt, a central node of the PI3K pathway, is frequently activated in a significant proportion of human solid tumors, making Akt an attractive target for therapeutic intervention. Akt inhibitors, which target the signaling pathway downstream of some of the most important growth factors and their tyrosine kinase receptors such as HER2, IGF1R, EGFR, and c-MET, should have broad utility against a wide array of human tumors. Utilizing a traditional compound screening approach, we have identified Akt inhibitors that block both the activation and kinase activity of the enzyme. Medicinal chemistry exploration of the structure activity relationships of these leads resulted in potent and selective Akt compounds including MK-2206. MK-2206 inhibits Akt isozymes 1, 2, and 3 with in vitro IC50 values of 8, 12, and 65 nM, respectively. MK-2206 is an allosteric inhibitor requiring the presence of the Pleckstrin homology domain for activity, and therefore is highly selective against Akt exhibiting no inhibitory activities against over 250 protein kinases when tested at 1\#956;M. In multiple cancer cell lines, MK-2206 inhibited Akt1 kinase activity (IC50 \#8776; 20 nM), and blocked Akt2 and Akt3 activities with 2- to 6-fold less potency. MK-2206 inhibited auto-phosphorylation of both Akt T308 and S473, as well as prevented Akt-mediated phosphorylation of down-stream signaling molecules, including TSC2, PRAS40 and ribosomal S6 proteins. MK-2206 exhibited potent anti-proliferative activity against a number of cancer cell lines harboring one or more of the following genetic defects: 1) gene amplification resulting in constitutive activation of upstream receptor tyrosine kinases such as HER2, 2) a PI3KCA activating mutation, 3) inactivation of tumor suppressor PTEN, and 4) amplification and mutation of Akt itself. In addition, activation of the Ras pathway tended to predict non-response to MK-2206.[1]
MK-2206 is currently being studies in two Phase I trials, one in healthy volunteers (HV) and one in cancer patients. In the first-in-human HV trial, twenty-four healthy, male subjects participated in this Phase I randomized, double-blind, placebo-controlled, sequential-panel, multiple-period, rising single oral dose study. Eight (8) subjects were assigned to each of 3 panels (Panels A, B, and C) where in each treatment period in a panel the same 6 subjects received MK-2206 and 2 subjects received placebo after an overnight fast. The volunteers were administered single doses from 0.25 to 100 mg and blood samples were collected predose and at prespecified postdose time points for pharmacokinetic and pharmacodynamic (whole blood inhibition of phospho Akt) assays. Single doses of MK-2206, up to 100 mg, were found to be generally well tolerated. No serious clinical or laboratory adverse experience was reported. The most commonly reported adverse experiences were headache, common cold, and diarrhea. One subject was discontinued from the study due to the clinical adverse experience of blurry vision which resolved. There were no clinically meaningful changes in laboratory safety tests or ECG evaluations. No clinically significant hyperglycemia or hyperinsulinemia was seen in these subjects. Preliminary pharmacokinetic results found that orally administered MK-2206 was readily absorbed with a median Tmax of 6 to 8 hours. The median half-life was 55 to 78 hours. AUC0-\#8734; and Cmax displayed dose proportional behavior from 2-mg to 100-mg. Preliminary pharmacodynamic results found that single doses of 40-, 80- and 100-mg MK-2206 inhibited Akt in whole blood to a greater extent than placebo. Maximum Akt inhibition occurred at 6 hours postdose for both the 80- and 100-mg doses with mean plasma concentrations of >65 nM. There was evidence of Akt inhibition from 2 through 24 hours. In conclusion, MK-2206 was generally well tolerated following single dose administration to healthy subjects. MK-2206 displays dose proportional pharmacokinetics with clear evidence of Akt inhibition. Clinical development of MK-2206 in cancer patients is ongoing with a focus on tumors harboring PI3K pathway activation events.[1]
The serine/threonine kinase Akt lies at a critical signaling node downstream of phosphatidylinositol-3-kinase and is important in promoting cell survival and inhibiting apoptosis. An Akt inhibitor may be particularly useful for cancers in which increased Akt signaling is associated with reduced sensitivity to cytotoxic agents or receptor tyrosine kinase inhibitors. We evaluated the effect of a novel allosteric Akt inhibitor, MK-2206, in combination with several anticancer agents. In vitro, MK-2206 synergistically inhibited cell proliferation of human cancer cell lines in combination with molecular targeted agents such as erlotinib (an epidermal growth factor receptor inhibitor) or lapatinib (a dual epidermal growth factor receptor/human epidermal growth factor receptor 2 inhibitor). Complementary inhibition of erlotinib-insensitive Akt phosphorylation by MK-2206 was one mechanism of synergism, and a synergistic effect was found even in erlotinib-insensitive cell lines. MK-2206 also showed synergistic responses in combination with cytotoxic agents such as topoisomerase inhibitors (doxorubicin, camptothecin), antimetabolites (gemcitabine, 5-fluorouracil), anti-microtubule agents (docetaxel), and DNA cross-linkers (carboplatin) in lung NCI-H460 or ovarian A2780 tumor cells. The synergy with docetaxel depended on the treatment sequence; a schedule of MK-2206 dosed before docetaxel was not effective. MK-2206 suppressed the Akt phosphorylation that is induced by carboplatin and gemcitabine. In vivo, MK-2206 in combination with these agents exerted significantly more potent tumor inhibitory activities than each agent in the monotherapy setting. These findings suggest that Akt inhibition may augment the efficacy of existing cancer therapeutics; thus, MK-2206 is a promising agent to treat cancer patients who receive these cytotoxic and/or molecular targeted agents.[2]
Inhibition of the survival kinase Akt can trigger apoptosis, and also has been found to activate autophagy, which may confound tumor attack. In this study, we investigated regulatory mechanisms through which apoptosis and autophagy were modulated in tumor cells subjected to Akt inhibition by MK-2206, the first allosteric small molecule inhibitor of Akt to enter clinical development. In human glioma cells, Akt inhibition by MK-2206 or siRNA-mediated attenuation strongly activated autophagy, whereas silencing of eukaryotic elongation factor-2 (eEF-2) kinase, a protein synthesis regulator, blunted this autophagic response. Suppression of MK-2206-induced autophagy by eEF-2 silencing was accompanied by a promotion of apoptotic cell death. Similarly, siRNA-mediated inhibition of eEF-2 kinase potentiated the efficacy of MK-2206 against glioma cells. Together, these results showed that blunting autophagy and augmenting apoptosis by inhibition of eEF-2 kinase could modulate the sensitivity of glioma cells to Akt inhibition. Our findings suggest that targeting eEF-2 kinase may reinforce the antitumor efficacy of Akt inhibitors such as MK-2206.[3]
*注: 文献方法仅供参考, InvivoChem并未独立验证这些方法的准确性
化学信息 & 存储运输条件
分子式
C₂₅H₂₂CLN₅O
分子量
443.93
精确质量
443.151
元素分析
C, 67.64; H, 5.00; Cl, 7.99; N, 15.78; O, 3.60
CAS号
1032349-77-1
相关CAS号
MK-2206 dihydrochloride;1032350-13-2;MK-2206 free base;1032349-93-1
PubChem CID
67254077
外观&性状
Solid powder
LogP
6.157
tPSA
89.33
氢键供体(HBD)数目
3
氢键受体(HBA)数目
4
可旋转键数目(RBC)
3
重原子数目
32
分子复杂度/Complexity
760
定义原子立体中心数目
0
SMILES
O=C1NN=C2C3C=C(C4C=CC=CC=4)C(C4C=CC(=CC=4)C4(CCC4)N)=NC=3C=CN21
InChi Key
LFYOZCBFOSSLNJ-UHFFFAOYSA-N
InChi Code
InChI=1S/C25H21N5O.ClH/c26-25(12-4-13-25)18-9-7-17(8-10-18)22-19(16-5-2-1-3-6-16)15-20-21(27-22)11-14-30-23(20)28-29-24(30)31;/h1-3,5-11,14-15H,4,12-13,26H2,(H,29,31);1H
化学名
8-(4-(1-aminocyclobutyl)phenyl)-9-phenyl-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3(2H)-one hydrochloride
别名
MK2206; MK-2206 hydrochloride; 1032349-77-1; MK-2206 Monohydrochloride; UNII-4HA45S22ZZ; 4HA45S22ZZ; 1,2,4-Triazolo(3,4-f)(1,6)naphthyridin-3(2H)-one, 8-(4-(1-aminocyclobutyl)phenyl)-9-phenyl-, hydrochloride (1:1); 8-[4-(1-aminocyclobutyl)phenyl]-9-phenyl-2H-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3-one;hydrochloride; MK2206; MK 2206
HS Tariff Code
2934.99.9001
存储方式

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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)
溶解度数据
溶解度 (体外实验)
Typically soluble in DMSO (e.g. > 10 mM)
溶解度 (体内实验)
注意: 如下所列的是一些常用的体内动物实验溶解配方,主要用于溶解难溶或不溶于水的产品(水溶度<1 mg/mL)。 建议您先取少量样品进行尝试,如该配方可行,再根据实验需求增加样品量。

注射用配方
(IP/IV/IM/SC等)
注射用配方1: DMSO : Tween 80: Saline = 10 : 5 : 85 (如: 100 μL DMSO 50 μL Tween 80 850 μL Saline)
*生理盐水/Saline的制备:将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中,得到澄清溶液。
注射用配方 2: DMSO : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (如: 100 μL DMSO 400 μL PEG300 50 μL Tween 80 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如: 100 μL DMSO 900 μL Corn oil)
示例: 注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液,加到 900 μL Corn oil/玉米油中, 混合均匀。
View More

注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如:100 μL DMSO 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备(4°C,储存1周):将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中,得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如: 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精) 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如: 50 μL DMSO 100 μL PEG300 200 μL Castor oil 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10: 10 : 80 (如: 100 μL Ethanol 100 μL Cremophor 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如: 100 μL EtOH 900 μL Corn oil)
注射用配方 10: EtOH : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (如: 100 μL EtOH 400 μL PEG300 50 μL Tween 80 450 μL Saline)


口服配方
口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中,得到0.5%CMC-Na澄清溶液;然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中,得到悬浮液。
View More

口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合


注意: 以上为较为常见方法,仅供参考, InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型,对于某些尚未有文献报道溶解方法的化合物,需通过前期实验来确定(建议先取少量样品进行尝试),包括产品的溶解情况、梯度设置、动物的耐受性等。

请根据您的实验动物和给药方式选择适当的溶解配方/方案:
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 2.2526 mL 11.2630 mL 22.5261 mL
5 mM 0.4505 mL 2.2526 mL 4.5052 mL
10 mM 0.2253 mL 1.1263 mL 2.2526 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。

计算器

摩尔浓度计算器可计算特定溶液所需的质量、体积/浓度,具体如下:

  • 计算制备已知体积和浓度的溶液所需的化合物的质量
  • 计算将已知质量的化合物溶解到所需浓度所需的溶液体积
  • 计算特定体积中已知质量的化合物产生的溶液的浓度
使用摩尔浓度计算器计算摩尔浓度的示例如下所示:
假如化合物的分子量为350.26 g/mol,在5mL DMSO中制备10mM储备液所需的化合物的质量是多少?
  • 在分子量(MW)框中输入350.26
  • 在“浓度”框中输入10,然后选择正确的单位(mM)
  • 在“体积”框中输入5,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案17.513 mg出现在“质量”框中。以类似的方式,您可以计算体积和浓度。

稀释计算器可计算如何稀释已知浓度的储备液。例如,可以输入C1、C2和V2来计算V1,具体如下:

制备25毫升25μM溶液需要多少体积的10 mM储备溶液?
使用方程式C1V1=C2V2,其中C1=10mM,C2=25μM,V2=25 ml,V1未知:
  • 在C1框中输入10,然后选择正确的单位(mM)
  • 在C2框中输入25,然后选择正确的单位(μM)
  • 在V2框中输入25,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案62.5μL(0.1 ml)出现在V1框中
g/mol

分子量计算器可计算化合物的分子量 (摩尔质量)和元素组成,具体如下:

注:化学分子式大小写敏感:C12H18N3O4  c12h18n3o4
计算化合物摩尔质量(分子量)的说明:
  • 要计算化合物的分子量 (摩尔质量),请输入化学/分子式,然后单击“计算”按钮。
分子质量、分子量、摩尔质量和摩尔量的定义:
  • 分子质量(或分子量)是一种物质的一个分子的质量,用统一的原子质量单位(u)表示。(1u等于碳-12中一个原子质量的1/12)
  • 摩尔质量(摩尔重量)是一摩尔物质的质量,以g/mol表示。
/

配液计算器可计算将特定质量的产品配成特定浓度所需的溶剂体积 (配液体积)

  • 输入试剂的质量、所需的配液浓度以及正确的单位
  • 单击“计算”按钮
  • 答案显示在体积框中
动物体内实验配方计算器(澄清溶液)
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)
第二步:请输入动物体内配方组成(配方适用于不溶/难溶于水的化合物),不同的产品和批次配方组成不同,如对配方有疑问,可先联系我们提供正确的体内实验配方。此外,请注意这只是一个配方计算器,而不是特定产品的确切配方。
+
+
+

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) 。

临床试验信息
Study of MK 2206 in Patients With Relapsed or Refractory Diffuse Large B Cell Lymphoma
CTID: NCT01466868
Phase: Phase 2
Status: Terminated
Date: 2014-07-10
Dose Defining Study For MK-2206 Combined With Gefitinib In Non Small Cell Lung Cancer (NSCLC)
CTID: NCT01147211
Phase: Phase 1
Status: Unknown status
Date: 2013-05-03
相关产品
联系我们