(S)-PI3Kα-IN-4
目录号 : GC62450
(S)-PI3Kα-IN-4 是一种有效的 PI3Kα 抑制剂，IC50 为 2.3 nM。(S)-PI3Kα-IN-4 对 PI3Kα 的选择性分别比 PI3Kβ，PI3Kδ 和 PI3Kγ 高38.3，4.25 和 4.93 倍。(S)-PI3Kα-IN-4 可用于癌症的研究。
Cas No.:2322293-84-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
(S)-PI3Kα-IN-4 is a potent inhibitor of PI3Kα, with an IC50 of 2.3 nM. (S)-PI3Kα-IN-4 shows 38.3-, 4.25-, and 4.93-fold selectivity for PI3Kα over PI3Kβ, PI3Kδ, and PI3Kγ, respectively. (S)-PI3Kα-IN-4 can be used for the research of cancer[1].
(S)-PI3Kα-IN-4 (compound 11) is a quinazolin-4(3H)-one derivative with 2-substituted-N-methylpropanamide substitution[1].
[1]. Dong J, et, al. Discovery of 3-Quinazolin-4(3 H)-on-3-yl-2, N-dimethylpropanamides as Orally Active and Selective PI3Kα Inhibitors. ACS Med Chem Lett. 2020 Jun 10;11(7):1463-1469.
| Cas No. | 2322293-84-3 | SDF | |
| 分子式 | C25H23ClFN5O5S | 分子量 | 560 |
| 溶解度 | 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 | 1.7857 mL | 8.9286 mL | 17.8571 mL |
| 5 mM | 0.3571 mL | 1.7857 mL | 3.5714 mL |
| 10 mM | 0.1786 mL | 0.8929 mL | 1.7857 mL |
| 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） | ||||||||||
| 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.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Finkelstein'S Test Is Superior to Eichhoff'S Test in the Investigation of de Quervain'S Disease
J Hand Microsurg 2018 Aug;10(2):116-118.PMID:30154628DOI:10.1055/s-0038-1626690.
Introduction de Quervain'S tenosynovitis is a common pathologic condition of the hand. Finkelstein'S test has long been considered to be a pathognomonic sign of this diagnosis, yet most clinicians and instruction manuals erroneously describe what is in fact the Eichhoff'S test, which is thought to produce similar pain by tendon stretching in a normal wrist. The purpose of this study was to compare Finkelstein'S test with Eichhoff'S test in asymptomatic individuals. Materials and Methods Thirty-six asymptomatic participants (72 wrists) were examined using both Finkelstein'S and Eichhoff'S tests with a minimum interval of 24 hours between the tests. Results The results showed that Finkelstein'S test was more accurate than Eichhoff'S test. It demonstrated higher specificity, produced significantly fewer numbers of false-positive results, and also caused significantly less discomfort to patients. Conclusion This study recommends Finkelstein'S test as the clinical examination of choice for the diagnosis of de Quervain'S disease.
Craniometrics and Ventricular Access: A Review of Kocher'S, Kaufman'S, Paine'S, Menovksy'S, Tubbs', Keen'S, Frazier'S, Dandy'S, and Sanchez'S Points
Oper Neurosurg (Hagerstown) 2020 May 1;18(5):461-469.PMID:31420653DOI:10.1093/ons/opz194.
Intraventricular access is frequently required during neurosurgery, and when neuronavigation is unavailable, the neurosurgeon must rely upon craniometrics to achieve successful ventricular cannulation. In this historical review, we summarize the most well-described ventricular access points: Kocher'S, Kaufman'S, Paine'S, Menovksy'S, Tubbs', Keen'S, Frazier'S, Dandy'S, and Sanchez'S. Additionally, we provide multiview, 3-dimensional illustrations that provide the reader with a novel understanding of the craniometrics associated with each point.
Algorithmic approach to find S -consistency in Common-Edge signed graph
MethodsX 2022 Jul 21;9:101783.PMID:35942208DOI:10.1016/j.mex.2022.101783.
Common-Edge signed graph C E ( S ) of a signed graph S is a signed graph whose vertex-set is the pairs of adjacent edges in S and two vertices are adjacent if the corresponding pairs of adjacent edges of S have exactly one edge in common, with the sign same as that of Common-Edge. S -Marked signed graph T is a signed graph which receives the marking μ due to the signed graph S called marker. Further, T is S -consistent if a marker S is defined and if S -marking μ of T with respect to which marked signed graph T μ is consistent. In this paper, we give an algorithm to detect if C E ( S ) is S -consistent or not and determine its complexity. • Algorithm to detect if C E ( S ) is S -consistent or not. • Determination of algorithm'S complexity.
(S,S)-formoterol increases the production of IL-4 in mast cells and the airways of a murine asthma model
Int Arch Allergy Immunol 2004 Apr;133(4):380-8.PMID:15031612DOI:10.1159/000077358.
Background: Racemic formoterol is an equimolar mixture of (R,R)- and (S,S)-formoterol. Several studies have shown (S,S)-formoterol to have proinflammatory effects. We previously reported that (S)-albuterol increased the secretion of histamine and interleukin (IL)-4 in murine mast cells. We thus hypothesized that (S,S)-formoterol promotes asthma by enhancing IL-4 production in mast cells of the asthmatic airway. Methods: Murine and human mast cells were stimulated by high affinity IgE receptor (Fc epsilon RI) cross-linking or with phorbol myristate acetate/calcium ionophore A23187 (PMA/A23187). Jurkat T cells were stimulated with PMA. Cells were pretreated with either (R,R)- or (S,S)-formoterol. Ovalbumin (OVA)-sensitized BALB/c mice were pretreated with (R,R)- or (S,S)-formoterol before each intranasal OVA challenge for 10 days. Bronchoalveolar lavage fluid was obtained from the mice. The levels of IL-4, histamine and PGD(2) were measured. Early and late allergic responses (EAR and LAR, respectively) to OVA challenge and airway hyperresponsiveness (AHR) were measured. Results: (S,S)-formoterol enhanced the production of IL-4, histamine, and PGD(2) in mast cells, whereas (R,R)-formoterol had no effect. Neither (S,S)- nor (R,R)-formoterol had effect on IL-4 production in Jurkat T cells. In OVA-challenged mice, (S,S)-formoterol increased IL-4 secretion, whereas (R,R)-formoterol had no effect. Finally, (S,S)-formoterol enhanced the inflammatory changes in the peribronchial and perivascular areas without affecting EAR, LAR or AHR, whereas (R,R)-formoterol reduced EAR, LAR and AHR as well as cellular infiltration in the lung tissue of these mice. Conclusion: (S,S)-formoterol may exert adverse effects in asthma control by activating mast cells to produce proinflammatory mediators such as IL-4.
Molecular mechanism of the S-RNase-based gametophytic self-incompatibility in fruit trees of Rosaceae
Breed Sci 2016 Jan;66(1):116-21.PMID:27069396DOI:10.1270/jsbbs.66.116.
Self-incompatibility (SI) is a major obstacle for stable fruit production in fruit trees of Rosaceae. SI of Rosaceae is controlled by the S locus on which at least two genes, pistil S and pollen S, are located. The product of the pistil S gene is a polymorphic and extracellular ribonuclease, called S-RNase, while that of the pollen S gene is a protein containing the F-box motif, SFB (S haplotype-specific F-box protein)/SFBB (S locus F-box brothers). Recent studies suggested that SI of Rosaceae includes two different systems, i.e., Prunus of tribe Amygdaleae exhibits a self-recognition system in which its SFB recognizes self-S-RNase, while tribe Pyreae (Pyrus and Malus) shows a non-self-recognition system in which many SFBB proteins are involved in SI, each recognizing subset of non-self-S-RNases. Further biochemical and biological characterization of the S locus genes, as well as other genes required for SI not located at the S locus, will help our understanding of the molecular mechanisms, origin, and evolution of SI of Rosaceae, and may provide the basis for breeding of self-compatible fruit tree cultivars.