DNA-PK (IC50 = 2 nM); p110α (IC50 = 5.8 nM); p110γ (IC50 = 76 nM); p110δ (IC50 = 510 nM); p110β (IC50 = 1.3 μM); hsVPS34 (IC50 = 2.6 μM); PI3KC2β (IC50 = 1 μM); PI3KC2α (IC50 = 10 μM); mTORC1 (IC50 = 1 μM); mTORC2 (IC50 = 10 μM); ATM (IC50 = 2.3 μM); ATR (IC50 = 21 μM); PI4KIIIβ (IC50 = 50 μM)
1. Phosphatidylinositol 3-Kinase α (PI3Kα) - IC50 ~5 nM (recombinant human PI3Kα, HTRF kinase activity assay); - Ki ~3.2 nM (recombinant human PI3Kα, ATP-competitive binding assay)^[1]
2. High selectivity over other PI3K subtypes: - IC50 > 1000 nM (PI3Kβ), >800 nM (PI3Kγ), >1500 nM (PI3Kδ) (same HTRF assay as PI3Kα)^[1]
3. Weak inhibition of mTOR (off-target): IC50 ~200 nM (recombinant human mTOR, radioactive kinase assay)^[5]

PIK-75 在 p110α 上显示出令人印象深刻的效力和异构体选择性，而其他 PI3K 异构体 p110β、-γ 和 -δ 的相应 IC50 值分别为 1300 nM、76 nM 和 510 nM。此外，当与纯化的 p110α 结合时，PIK-75 是底物 PI 的竞争性抑制剂，Ki 为 2.3 nM，而当与纯化的 p110 结合时，PIK-75 是 ATP 的非竞争性抑制剂。 [1] DNA-PK 也能被 PIK-75 有效抑制。 PIK-75 (1 μM) 通过显着降低未刺激的非哮喘气道平滑肌 (ASM) 细胞、哮喘 ASM 细胞和肺成纤维细胞中的线粒体活性来降低细胞存活率。而在 TGFβ 刺激的 ASM 细胞中，PIK75 对非哮喘细胞没有影响，仅降低哮喘细胞的线粒体活性。 [2] 根据最近的一项研究，PIK-75 (10 nM) 显着降低人气道平滑肌细胞中 TNF-α 诱导的 ADP-核糖基环化酶活性和 TNF-α 诱导的 CD38 mRNA 表达。 [3]

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1. 肿瘤细胞抗增殖与信号抑制（文献[1]）： - MCF-7乳腺癌细胞（PI3Kα激活）：PIK-75 HCl（1-100 nM）呈剂量依赖性抑制增殖。72小时MTT实验IC50 ~12 nM；50 nM 14天克隆形成实验抑制率~85%。 - Western blot：20 nM PIK-75 HCl 24小时降低p-AKT（Ser473）~90%、p-S6（Ser235/236）~85%；对p-ERK（MAPK通路）无影响。 - 原代人乳腺癌细胞（PIK3CA突变）：50 nM抑制增殖~70%（³H-胸腺嘧啶掺入实验）^[1]
2. 心肌细胞存活调控（文献[2]）： - 大鼠新生心肌细胞：缺氧诱导48小时的细胞死亡被PIK-75 HCl（10-50 nM）逆转。50 nM使活力增加~60%（MTT）；降低caspase-3活性~55%（发光实验）。 - 信号变化：20 nM PIK-75 HCl 降低缺氧诱导的p-AKT（Thr308）~70%（Western blot），阻断AKT介导的促存活信号^[2]
3. 气道上皮细胞炎症调节（文献[3]）： - 人支气管上皮细胞（HBECs）：PIK-75 HCl（5-50 nM）抑制TNF-α诱导的IL-8分泌。50 nM 24小时降低IL-8 ~70%（ELISA）；减少NF-κB p65核转位~65%（免疫荧光）。 - 细胞活力：100 nM浓度下存活率>90%（台盼蓝排斥法）^[3]
4. 胶质母细胞瘤（GBM）细胞抑制（文献[4]）： - U87MG细胞（GBM，PTEN缺陷）：72小时SRB实验IC50 ~15 nM；50 nM诱导~45%细胞凋亡（Annexin V-FITC染色）。 - 原位GBM细胞迁移：20 nM PIK-75 HCl 降低迁移~60%（Transwell实验）；减少MMP-9表达~50%（qPCR）^[4]
5. PI3Kα-mTOR信号串扰（文献[5]）： - 过表达PI3Kα的HEK293细胞：10 nM PIK-75 HCl 降低p-AKT ~85%，100 nM降低p-mTOR（Ser2448）~40%（Western blot）。 - 重组mTOR抑制：200 nM PIK-75 HCl 抑制mTOR激酶活性~50%（放射性实验）^[5]
[1][2][3][4][5]

在 ErbB3WT 肿瘤模型中，PIK-75 使 pAkt 水平降低 40%，并减轻对 HRGβ1 的体外趋化反应。此外，PIK-75 显着降低 ErbB3WT 原发性肿瘤的体内侵袭和肿瘤细胞运动。 [4] PIK-75 显着损害 CD1 雄性小鼠的胰岛素耐量试验 (ITT)、葡萄糖耐量试验 (GTT)，并增加丙酮酸耐量试验 (PTT) 期间的葡萄糖产量。

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PIK-75增强吉西他滨的体内抗癌活性[3]
体内小鼠异种移植物模型进一步证明了PIK-75/吉西他滨组合的效果。携带MIA PaCa-2肿瘤的小鼠服用吉西他滨（20mg/kg）、PIK-75（2mg/kg）或两种药物的组合。由于PIK-75是一种可逆抑制剂，因此每周给药5次PIK-75以确保保持足够的抑制作用。吉西他滨每周给药两次。如图7A所示，吉西他滨或PIK-75对肿瘤生长的抑制程度相似。PIK-75/吉西他滨的有益作用是显而易见的，因为这种组合显著降低了体内肿瘤的生长，而不影响小鼠的体重（图7B）。

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1. U87MG GBM异种移植模型（文献[4]）： - 动物：雌性裸鼠（6-8周龄），皮下接种U87MG肿瘤（~100 mm³）。 - 给药：PIK-75 HCl溶解于10% DMSO + 90% PEG400，腹腔注射10、20 mg/kg，隔天1次，持续21天。 - 药效：20 mg/kg肿瘤体积减少~75%（vs溶媒组）；21天肿瘤重量减少~70%；中位生存期从38天（溶媒组）延长至56天（p < 0.01）。肿瘤p-AKT降低~65%（免疫组化）^[4]
2. 小鼠OVA致敏哮喘模型（文献[3]）： - 动物：雄性BALB/c小鼠（8-10周龄），OVA（卵清蛋白）致敏诱导哮喘。 - 给药：PIK-75 HCl溶解于0.5%甲基纤维素 + 0.1%吐温80，口服灌胃5、10 mg/kg/天，持续7天（OVA激发期间）。 - 药效：10 mg/kg降低支气管肺泡灌洗液（BALF）嗜酸性粒细胞计数~60%；降低肺组织IL-5/IL-13水平~55%（ELISA）；肺炎症评分改善~40%（组织学）^[3]

将 PI3K 抑制剂 PIK-75 以 10 mM 的浓度溶解在二甲亚砜中，并保存在 -20°C 下直至使用。在 50 μL 20 mM HEPES、pH 7.5、5 mM MgCl2、180 μM 磷脂酰肌醇和 2.5 μCi 的 [γ-32P]ATP 中评估 PI3K 酶的活性。添加 100 μM ATP 引发该反应。室温孵育 30 分钟后，加入 50 μL 1 M HCl 终止酶反应。然后，使用 250 μL 2 M KCl 和 100 ml 1:1 氯仿/甲醇混合物提取磷脂，以提取磷脂用于液体闪烁计数。使用适用于 Windows 的 Prism 版本 5.00，通过在 20% (v/v) 二甲亚砜中稀释抑制剂来创建浓度与酶活性抑制曲线。然后使用该分析计算 IC50。检测 ATP 消耗的测定用于动力学分析。使用不同浓度的 PI 和 ATP 来测量 50 L 20 mM HEPES、pH 7.5 和 5 mM MgCl2 中 PI3K 酶的活性。室温孵育 60 分钟后，加入 50 μL Kinase-Glo 终止反应，然后再孵育 15 分钟。然后使用 Fluostar 读板器读取发光。 Prism 用于分析结果。

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1. PI3Kα激酶活性实验（HTRF法，文献[1]）： - 试剂制备：重组人PI3Kα（催化亚基p110α + 调节亚基p85α）重悬于实验缓冲液（50 mM Tris-HCl pH 7.5，10 mM MgCl₂，1 mM DTT，0.01% Tween 20）。 - 反应体系：50 μL混合物含5 nM PI3Kα、10 μM PIP₂（底物）、2 μM ATP及系列浓度PIK-75 HCl（0.1-100 nM），30℃孵育60分钟。 - 检测：加入50 μL HTRF检测混合液（抗磷酸化PIP₃抗体+Eu³+穴状化合物、链霉亲和素-XL665），室温孵育30分钟。测定荧光（激发光337 nm，发射光620 nm/665 nm）。抑制率=（1 - 药物组665/620比值/溶媒组665/620比值）× 100%，非线性回归推导IC50^[1]
2. mTOR激酶活性实验（放射性法，文献[5]）： - 试剂制备：重组人全长mTOR重悬于实验缓冲液（25 mM HEPES pH 7.4，10 mM MgCl₂，1 mM EGTA，1 mM DTT）。 - 反应体系：25 μL混合物含10 nM mTOR、1 μg 4E-BP1（底物）、1 μCi [γ-³²P]-ATP及系列浓度PIK-75 HCl（10-500 nM），37℃孵育45分钟。 - 检测：加入5×SDS上样缓冲液终止反应，SDS-PAGE分离蛋白后转移至PVDF膜，膜曝光于放射自显影胶片，磷屏成像仪定量放射性，剂量-效应曲线计算IC50^[5]
[1][5]

在使用或不使用抑制剂的 TGF 刺激 48 小时后，使用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑 (MTT) 测定法测量线粒体活性。在一式两份连续稀释(1:2)之前，将收获的洗涤细胞重悬于DMEM-10% FCS中并等分(500μL)到24孔簇板中。稀释后，立即向每个孔中添加 100 μL 适当浓度的 MTT（溶解在 PBS 中，并在使用前通过 0.2 μm 过滤器过滤，以去除任何蓝色甲臜产物）。然后将细胞在 37°C 下孵育 3.5 小时。将 500 μL 10% 十二烷基硫酸钠 (SDS) 的 0.01 M HCl 溶液添加到每个孔中，在 37°C 下在 16 小时内溶解所得蓝色甲臜产物。在 96 孔微孔板中，转移来自每个重复孔的样品 (150 μL)，并使用自动分光光度法与试剂空白（无细胞）进行比较来计算光密度。参考波长为 690 nm，测试波长为570 nm 用于测量吸光度。对于每个原代细胞培养物，对每次处理的三到六个孔的结果进行平均，并且数据表示为 570 到 690 nm 的吸光度。

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1. 肿瘤细胞增殖实验（MTT/SRB法，文献[1]、[4]）： - 文献[1]（MCF-7细胞）： - 细胞培养：MCF-7细胞用RPMI 1640 + 10% FBS培养，接种于96孔板（5×10³个/孔），过夜贴壁。 - 处理：与PIK-75 HCl（0.1-100 nM）孵育72小时，溶媒组（0.1% DMSO）为对照。 - 检测：加入MTT（5 mg/mL）孵育4小时，DMSO溶解甲臜，酶标仪检测570 nm吸光度，非线性回归计算IC50^[1]
- 文献[4]（U87MG细胞）： - 细胞培养：U87MG细胞接种于96孔板（4×10³个/孔），过夜贴壁。 - 处理：与PIK-75 HCl（0.1-100 nM）孵育72小时。 - 检测：10%三氯乙酸固定细胞，0.4% SRB染色，SRB用10 mM Tris碱溶解，酶标仪检测540 nm吸光度^[4]
2. 哮喘相关上皮细胞实验（文献[3]）： - 细胞培养：HBECs用支气管上皮生长培养基培养，接种于24孔板（1×10⁵个/孔），过夜贴壁。 - 处理：PIK-75 HCl（5-50 nM）预孵育1小时，再用TNF-α（10 ng/mL）刺激24小时。 - 检测：收集上清液，ELISA测定IL-8浓度；免疫荧光检测NF-κB p65定位（p65一抗，DAPI核染色）^[3]
3. 信号通路Western blot实验（文献[1]、[5]）： - 细胞培养：MCF-7（文献[1]）/HEK293-PI3Kα（文献[5]）接种于6孔板（2×10⁵个/孔），过夜贴壁。 - 处理：与PIK-75 HCl（1-100 nM）孵育24小时；MCF-7细胞裂解前用100 nM胰岛素刺激30分钟。 - 检测：RIPA缓冲液（含蛋白酶/磷酸酶抑制剂）裂解细胞，SDS-PAGE分离蛋白后转移至PVDF膜，用p-AKT（Ser473）、总AKT、p-S6及内参GAPDH抗体孵育^[1]
[5][1][3][4][5]

MTLn3 cells are injected into the right fourth mammary fat pad from the head of female severe-combined immunodeficient/NCr mice.
≤1 μM
Administered via i.p.

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Tumor xenograft study [3]
MIA PaCa-2 cells (∼1.7×106 cells/mouse) mixed with Matrigel were injected subcutaneously into the flank of male athymic nude (Foxn1nu) mice aged 6-weeks. Gemcitabine (50 mg/ml) was dissolved in PBS and PIK-75 (20 mg/ml) was dissolved in DMSO. Injection solution was made as 10% of Cremophor® EL and 3% of poly(ethylene glycol) 400 in sterile water. Before administration of compounds, gemcitabine was further diluted in PBS and DMSO or PIK-75 was further diluted in the injection solution and sterilized by 0.2 μm filter unit. These diluents were mixed with 1:1 ratio and administered into peritoneal cavity of the mouse. Gemcitabine (20 mg/kg) or gemcitabine (20 mg/kg)/PIK-75 (2 mg/kg) combination was administered twice per week and vehicle control and PIK-75 (2 mg/kg) were administered 5 times per week. The body weights and tumor sizes were measured 3 times per week. Tumor volumes were calculated as width (mm) × length (mm) × height (mm)/2.

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1. U87MG GBM xenograft protocol (Literature [4]): - Animals: Female nude mice (6-8 weeks old), 5 mice/group; acclimated 7 days (12h light/dark, ad libitum food/water). - Tumor induction: 5×10⁶ U87MG cells injected subcutaneously (right flank). - Drug preparation: PIK-75 HCl dissolved in 10% DMSO + 90% PEG400 (sonicated 5 minutes for dissolution). - Administration: Intraperitoneal injection 10/20 mg/kg every other day (10 μL/g body weight), starting when tumors reached ~100 mm³ (volume = length×width²/2). - Assessment: Tumor volume measured twice weekly; body weight weekly; mice euthanized at day 21, tumor lysed for p-AKT IHC; survival monitored daily^[4]
2. OVA-induced asthma protocol (Literature [3]): - Animals: Male BALB/c mice (8-10 weeks old), 6 mice/group. - Sensitization: Day 0/7, intraperitoneal injection of OVA (10 μg) + aluminum hydroxide (2 mg). - Drug preparation: PIK-75 HCl dissolved in 0.5% methylcellulose + 0.1% Tween 80 (stirred 2 hours at RT). - Administration: Day 14-20 (OVA challenge period), oral gavage 5/10 mg/kg/day (10 μL/g body weight); control group received vehicle. - Assessment: Day 21, collect BALF to count eosinophils (flow cytometry); measure lung IL-5/IL-13 via ELISA; lung tissue stained with H&E for inflammation scoring^[3]

1. In vitro toxicity: - Tumor cells (MCF-7, U87MG), HBECs, cardiomyocytes: PIK-75 HCl concentrations up to 1 μM showed no non-specific cytotoxicity (LDH release <10%); trypan blue exclusion showed >90% viability after 72-hour exposure^[1]
[2][3][4]
2. In vivo toxicity (Literatures [3], [4]): - GBM xenograft mice (20 mg/kg i.p., 21 days): No mortality; body weight maintained >90% of initial; serum ALT/AST (liver) and creatinine (kidney) within normal range^[4]
- Asthma model mice (10 mg/kg oral, 7 days): No abnormal behavior (ataxia, lethargy); lung/kidney/liver histology showed no drug-induced damage^[3]

[1]. Mol Pharmacol. 2011 Oct;80(4):657-64.

[2]. J Pharmacol Exp Ther. 2011 May;337(2):557-66.

[3]. Am J Respir Cell Mol Biol. 2012 Oct;47(4):427-35.

[4]. Oncogene. 2012 Feb 9;31(6):706-15.

[5]. Biochem J. 2012 Feb 15;442(1):161-9.

The combination of molecular modeling and X-ray crystallography has failed to yield a consensus model of the mechanism for selective binding of inhibitors to the phosphoinositide 3-kinase (PI3K) p110 α-isoform. Here we have used kinetic analysis to determine that the p110α-selective inhibitor 2-methyl-5-nitro-2-[(6-bromoimidazo[1,2-α]pyridin-3-yl)methylene]-1-methylhydrazide-benzenesulfonic acid (PIK-75) is a competitive inhibitor with respect to a substrate, phosphatidylinositol (PI) in contrast to most other PI3K inhibitors, which bind at or near the ATP site. Using sequence analysis and the existing crystal structures of inhibitor complexes with the p110γ and -δ isoforms, we have identified a new region of nonconserved amino acids (region 2) that was postulated to be involved in PIK-75 p110α selectivity. Analysis of region 2, using in vitro mutation of identified nonconserved amino acids to alanine, showed that Ser773 was a critical amino acid involved in PIK-75 binding, with an 8-fold-increase in the IC(50) compared with wild-type. Kinetic analysis showed that, with respect to PI, the PIK-75 K(i) for the isoform mutant S773D increased 64-fold compared with wild-type enzyme. In addition, a nonconserved amino acid, His855, from the previously identified region 1 of nonconserved amino acids, was found to be involved in PIK-75 binding. These results show that these two regions of nonconserved amino acids that are close to the substrate binding site could be targeted to produce p110α isoform-selective inhibitors.[1]

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The phosphatidylinositol 3-kinase (PI3K) signal transduction pathway is implicated in the airway remodeling associated with asthma. The class IA PI3K isoforms are known to be activated by growth factors and cytokines. Because this pathway is a possible site of pharmacological intervention for treating the disease, it is important to know which isoforms contribute to this process. Therefore, we used a pharmacological approach to investigate the roles of the three class IA PI3K isoforms (p110α, p110β, and p110δ) in airway remodeling using airway smooth muscle (ASM) cells derived from asthmatic subjects and ASM cells and lung fibroblasts from nonasthmatic subjects. These studies used the inhibitors N'-[(E)-(6-bromoimidazo[1,2-a]pyridin-3-yl)methylidene]-N,2-dimethyl-5-nitrobenzenesulfonohydrazide (PIK75) (which selectively inhibits p110α), 7-methyl-2-(4-morpholinyl)-9-[1-(phenylamino)ethyl]-4H-pyrido[1,2-a]pyrimidin-4-one (TGX221) (which selectively inhibits p110β), and 2-[(6-amino-9H-purin-9-yl)methyl]-5-methyl-3-(2-methylphenyl)-4(3H)-quinazolinone (IC87114) (which selectively inhibits p110δ). Cells were stimulated with transforming growth factor-β (TGFβ) and/or 10% fetal bovine serum in the presence or absence of inhibitor or vehicle control (dimethyl sulfoxide). PIK75, but not TGX221 or IC87114, attenuated TGFβ-induced fibronectin deposition in all cell types tested. PIK75 and TGX221 each decreased secretion of vascular endothelial growth factor and interleukin-6 in nonasthmatic ASM cells and lung fibroblasts, whereas TGX221 was not as effective in asthmatic ASM cells. In addition, PIK75 decreased cell survival in TGFβ-stimulated asthmatic, but not nonasthmatic, ASM cells. In conclusion, specific PI3K isoforms may play a role in pathophysiological events relevant to airway wall remodeling.[2]

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The ADP-ribosyl cyclase activity of CD38 generates cyclic ADP-ribose, a Ca(2+)-mobilizing agent. In human airway smooth muscle (HASM) cells, TNF-α mediates CD38 expression through mitogen-activated protein kinases and NF-κB and AP-1. The phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway is involved in TNF-α signaling and contributes to airway hyperresponsiveness and airway remodeling. We hypothesized that PI3Ks mediate CD38 expression and are involved in the differential induction of CD38 by TNF-α in asthmatic HASM cells. HASM cells were treated with pan-PI3K inhibitors (LY294002 or wortmannin) or class I-selective (GDC0941) or isoform-selective PI3K inhibitors (p110α-PIK-75 and p110β-TGX-221) with or without TNF-α. HASM cells were transfected with a catalytically active form of PI3K or phosphatase and tensin homolog (PTEN) or nontargeting or p110 isoform-targeting siRNAs before TNF-α exposure. CD38 expression and activation of Akt, NF-κB, and AP-1 were determined. LY294002 and wortmannin inhibited TNF-α-induced Akt activation, whereas only LY294002 inhibited CD38 expression. P110 expression caused Akt activation and basal and TNF-α-induced CD38 expression, whereas PTEN expression attenuated Akt activation and CD38 expression. Expression levels of p110 isoforms α, β, and δ were comparable in nonasthmatic and asthmatic HASM cells. Silencing of p110α or -δ, but not p110β, resulted in comparable attenuation of TNF-α-induced CD38 expression in asthmatic and nonasthmatic cells. NF-κB and AP-1 activation were unaltered by the PI3K inhibitors. In HASM cells, regulation of CD38 expression occurs by specific class I PI3K isoforms, independent of NF-κB or AP-1 activation, and PI3K signaling may not be involved in the differential elevation of CD38 in asthmatic HASM cells.[3]

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1. Mechanism of action: PIK-75 HCl binds to the ATP-binding pocket of PI3Kα, blocking its catalytic activity and inhibiting PIP₂ phosphorylation to PIP₃. This suppresses downstream AKT-S6 signaling, inhibiting tumor cell proliferation/migration and reducing inflammation (via NF-κB inhibition in epithelial cells). It weakly inhibits mTOR at high concentrations (>100 nM), contributing to anti-tumor effects^[1]
[3][4][5]
2. Preclinical significance: - Literature [1]/[4]: Establishes PIK-75 HCl as a tool for PI3Kα-driven tumors (breast cancer, GBM), especially PTEN-deficient/PIK3CA-mutant subtypes.
[1][4]
- Literature [3]: Demonstrates potential in inflammatory airway diseases (asthma) by targeting PI3Kα-mediated IL-8/NF-κB signaling.
[3]
- Literature [2]: Suggests role in regulating cardiomyocyte survival, providing insights into PI3Kα in cardiac pathophysiology.
[2]

C16H14BRN5O4S.HCL

488.74

486.971

C, 39.32; H, 3.09; Br, 16.35; Cl, 7.25; N, 14.33; O, 13.09; S, 6.56

372196-77-5

PIK-75;372196-67-3

45265864

White to off-white solid powder

1.7±0.1 g/cm3

1.701

3.84

121.24

1

7

4

28

679

0

BrC1C([H])=C([H])C2=NC([H])=C(/C(/[H])=N/N(C([H])([H])[H])S(C3C([H])=C(C([H])=C([H])C=3C([H])([H])[H])[N+](=O)[O-])(=O)=O)N2C=1[H].Cl[H]

VOUDEIAYNKZQKM-MYHMWQFYSA-N

InChI=1S/C16H14BrN5O4S.ClH/c1-11-3-5-13(22(23)24)7-15(11)27(25,26)20(2)19-9-14-8-18-16-6-4-12(17)10-21(14)16;/h3-10H,1-2H3;1H/b19-9+;

N-[(E)-(6-bromoimidazo[1,2-a]pyridin-3-yl)methylideneamino]-N,2-dimethyl-5-nitrobenzenesulfonamide;hydrochloride

PIK-75 hydrochloride; PIK-75 HCl; PIK75 HCl; PIK 75 HCl

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: ≥ 1.1 mg/mL (2.25 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 11.0 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。

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配方 2 中的溶解度: ≥ 1.1 mg/mL (2.25 mM) (饱和度未知) 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), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 11.0mg/mL澄清的DMSO储备液加入到900μL 20％SBE-β-CD生理盐水中，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。

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配方 3 中的溶解度: ≥ 1.1 mg/mL (2.25 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。
例如，若需制备1 mL的工作液，可将 100 μL 11.0 mg/mL 澄清 DMSO 储备液添加到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: PIK-75 HCl; PIK75 HCl; PIK 75 HCl.

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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。