EGFR tyrosine kinase
Gefitinib hydrochloride (Gefitinib) targets epidermal growth factor receptor (EGFR) tyrosine kinase (IC₅₀ = 0.033 μM for EGFR kinase activity; IC₅₀ = 0.054 μM for inhibiting EGF-stimulated tumor cell growth) [1]
Gefitinib hydrochloride (Gefitinib) targets human epidermal growth factor receptor 2 (HER2) and inhibits HER2-driven signaling in HER2-overexpressing tumor cells [3]
Gefitinib hydrochloride (Gefitinib) targets wild-type EGFR and mutant EGFRvIII: it inhibits wild-type EGFR-mediated phosphorylation, proliferation and anchorage-independent growth at low concentrations; for EGFRvIII-expressing cells, low concentrations (0.01-0.1 μM) increase EGFRvIII phosphotyrosine load and downstream ERK signaling, while high concentrations (1-2 μM) inhibit EGFRvIII-mediated activities [2]

长期暴露于表达 EGFRvIII 的细胞后，吉非替尼 (0.01-0.1 mM) 会增加受体的磷酸酪氨酸负载，增加 ERK 信号传导，并刺激增殖和贴壁依赖性生长。这种效应可能是由 EGFRvIII 二聚化的诱导引起的。相反，吉非替尼 (1-2 mM) 均显着降低 EGFRvIII 磷酸酪氨酸负荷、EGFRvIII 介导的增殖和锚定非依赖性生长[1]。吉非替尼 (ZD1839) 的 IC50 为 20 nM，可防止这些 EGF 驱动的未转化细胞生长单层[2]。吉非替尼的 IC50 为 2 μM，可抑制 GLC82 和 CALU-3 细胞的生长[3]。

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表皮生长因子受体（EGFR）在许多人类肿瘤中经常被扩增和/或突变，并且来自该受体的异常信号被认为是导致这些肿瘤中出现恶性表型的原因。吉非替尼是一种特异性结合和抑制EGFR酪氨酸激酶的小分子抑制剂，已被证明可以抑制一系列过表达EGFR的肿瘤细胞的生长、增殖、存活和侵袭。然而，吉非替尼的临床反应与EGFR水平和活性没有相关性，这表明下游信号传导和突变等其他分子机制在预测临床反应方面可能很重要。因此，我们研究了特异性EGFR抑制剂吉非替尼对表达天然存在的组成型活性EGFR变体EGFRvIII、低非转化水平EGFR和高转化水平EGFR的细胞的磷酸化水平、信号传导和生长的影响。结果显示，在表达EGFRvIII的细胞中，吉非替尼足以抑制EGFR磷酸化、EGFR介导的增殖和EGFR-介导的锚定非依赖性生长的水平不足以抑制这些特征。此外，数据表明，表达EGFRvIII的细胞长期暴露于低浓度吉非替尼（0.01-0.1微M）会导致受体磷酸酪氨酸负荷增加，ERK信号传导增加，并刺激增殖和锚定非依赖性生长，可能是通过诱导EGFRvⅢ二聚化。另一方面，较高浓度的吉非替尼（1-2微M）显著降低了EGFRvIII磷酸酪氨酸负荷、EGFRvⅢ介导的增殖和锚定非依赖性生长。需要进一步的研究来调查这些重要发现在临床环境中的意义。[2]

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表皮生长因子受体（EGFR）在许多人类肿瘤中普遍过表达，为抗癌药物开发提供了新的靶点。ZD1839（“易瑞沙”）是一种对EGFR具有选择性的喹唑啉酪氨酸激酶抑制剂，在临床前研究和临床试验的早期阶段显示出良好的活性。然而，由于尚不清楚哪种肿瘤类型是该药物治疗的最佳靶点，因此已经研究了与ZD1839肿瘤敏感性相关的分子特征。在一组人类乳腺癌症和其他上皮肿瘤细胞系中，HER2-过表达肿瘤对ZD1839特别敏感。这些肿瘤细胞系的生长抑制与EGFR、HER2和HER3的去磷酸化有关，同时HER3与磷脂酰肌醇3-激酶的结合丧失，Akt活性下调。这些研究表明，HER2过表达的肿瘤特别容易受到HER家族酪氨酸激酶信号传导的抑制，并提出了治疗这些特别侵袭性肿瘤的新策略。[3]

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1. 吉非替尼盐酸盐（Gefitinib hydrochloride）可强效抑制EGFR酪氨酸激酶活性（IC₅₀=0.033μM），并选择性抑制EGF刺激的肿瘤细胞增殖（IC₅₀=0.054μM）；同时可阻断肿瘤细胞中EGF诱导的EGFR自磷酸化，证实其对EGFR信号通路的靶点特异性抑制作用[1]
2. 在表达野生型EGFR的细胞（NR6wtEGFR，低EGFR表达；NR6W，高EGFR表达）中，吉非替尼盐酸盐（Gefitinib hydrochloride）低浓度即可抑制EGF诱导的EGFR磷酸化（涉及Tyr845、Tyr992、Tyr1045、Tyr1068、Tyr1086、Tyr1148、Tyr1173位点）、下游信号分子（p-ERK、p-PLC-γ、p-AKT、p-STAT3）激活及细胞增殖；在表达EGFRvIII的NR6M细胞中，该化合物低浓度（0.01-0.1μM）会增加EGFRvIII磷酸化水平、增强ERK信号、促进细胞增殖及锚定非依赖性生长（可能通过诱导EGFRvIII二聚化），高浓度（1-2μM）则显著降低EGFRvIII磷酸化，抑制其介导的增殖和锚定非依赖性生长[2]
3. 吉非替尼盐酸盐（Gefitinib hydrochloride）可抑制HER2过表达的乳腺癌及上皮肿瘤细胞系生长，这种生长抑制与EGFR、HER2、HER3的去磷酸化、HER3与磷脂酰肌醇3-激酶（PI3K）结合减少及Akt活性下调相关[3]
4. 在LKB1野生型非小细胞肺癌（NSCLC）细胞系中，吉非替尼盐酸盐（Gefitinib hydrochloride）与二甲双胍联用呈现协同抗增殖和促凋亡作用：二甲双胍单独使用会通过增加C-RAF/B-RAF异源二聚化激活丝裂原活化蛋白激酶（MAPK），而吉非替尼盐酸盐（Gefitinib hydrochloride）可抑制EGFR磷酸化及下游信号，阻断二甲双胍诱导的MAPK激活，进而增强凋亡效应[4]
5. 吉非替尼盐酸盐（Gefitinib hydrochloride）可抑制辐射损伤大鼠来源的肺成纤维细胞增殖及EGFR表达，这一作用有助于减轻辐射诱导的肺纤维化；但同时会增加辐射大鼠肺内炎症细胞浸润及促炎细胞因子（IL-6、IL-1β）产生[5]

当皮下培养作为肿瘤异种移植物的含有H1299或CALU-3 GEF-R细胞的裸鼠给予二甲双胍和吉非替尼（150 mg/kg，口服）时，肿瘤生长显着减少[3]。虽然吉非替尼治疗由于肺成纤维细胞增殖减少而减弱纤维化肺重塑，但它增加了受辐射大鼠的肺部炎症，包括炎症细胞浸润和促炎细胞因子表达[4]。

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在对携带一系列人类肿瘤衍生异种移植物的小鼠的研究中，每天口服一次ZD1839以剂量依赖的方式抑制肿瘤生长。EGFR的表达水平并不能决定异种移植物肿瘤对ZD1839的敏感性。长期ZD1839（>3个月）治疗携带A431异种移植物的小鼠具有良好的耐受性，ZD1839完全抑制了肿瘤生长并诱导了已建立肿瘤的消退。ZD1839治疗期间没有出现耐药性肿瘤，但一些肿瘤在停药后复发。这些研究表明ZD1839在治疗许多人类肿瘤方面的潜在效用，并表明每天口服一次可能是一种合适的治疗方案。[1]

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吉非替尼治疗在第15天和第57天增加了受照射大鼠肺部炎性细胞的浸润，这些细胞会产生更多的促炎细胞因子（IL-6、IL-1β），而吉非替宁治疗在第57天降低了受照射的大鼠肺部胶原蛋白含量，并降低了受照大鼠肺部成纤维细胞的增殖和EGFR表达。 结论：在受照射的大鼠中，吉非替尼治疗增强了肺部炎症，包括炎性细胞浸润和促炎细胞因子表达，而吉非替宁治疗由于抑制肺成纤维细胞增殖而减轻了纤维化肺重塑[5]。

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1. 在接种多种人源肿瘤异种移植瘤（包括A431细胞）的裸鼠中，每日口服一次吉非替尼盐酸盐（Gefitinib hydrochloride）可呈剂量依赖性抑制肿瘤生长（测试剂量：3.125-200mg/kg）；长期治疗（>3个月）耐受性良好，可完全抑制A431异种移植瘤生长并诱导已形成肿瘤消退；治疗期间未出现耐药肿瘤，但部分肿瘤在停药后复发[1]
2. 在NSCLC小鼠异种移植模型中，吉非替尼盐酸盐（Gefitinib hydrochloride）与二甲双胍联用相比单独使用任一药物，对肿瘤生长的抑制作用更强，证实该联用在LKB1野生型NSCLC中的体内协同抗肿瘤效应[4]
3. 在经胸腔单次20Gy X射线照射造成肺损伤的Wistar大鼠中，从照射后第1天至第14天口服给予吉非替尼盐酸盐（Gefitinib hydrochloride）（50mg/kg/天）：第15天时，大鼠肺内炎症细胞浸润增加，促炎细胞因子（IL-6、IL-1β）水平升高；第57天时，肺胶原含量减少，肺成纤维细胞增殖受抑，纤维化肺重构得到缓解[5]

1. EGFR酪氨酸激酶活性检测：将重组EGFR酪氨酸激酶结构域与系列浓度的吉非替尼盐酸盐（Gefitinib hydrochloride）在ATP及EGFR特异性肽底物存在下共同孵育。在适宜温度下孵育设定时间后，采用合适方法（如免疫印迹或激酶活性检测试剂盒）检测肽底物的磷酸化水平，计算抑制率并确定吉非替尼盐酸盐（Gefitinib hydrochloride）对EGFR激酶活性的IC₅₀值[1]
2. EGFR/EGFRvIII磷酸化检测：将表达野生型EGFR（NR6wtEGFR、NR6W）或突变型EGFRvIII（NR6M）的细胞用不同浓度的吉非替尼盐酸盐（Gefitinib hydrochloride）处理；对需EGF刺激的细胞，药物预处理后加入10nM EGF。制备全细胞裂解液，用磷酸化特异性抗体通过免疫印迹检测EGFR/EGFRvIII特定酪氨酸位点（Tyr845、Tyr992、Tyr1045、Tyr1068、Tyr1086、Tyr1148、Tyr1173）的磷酸化水平；检测总EGFR/EGFRvIII水平作为内参，对条带强度进行定量以评估化合物对受体磷酸化的影响[2]
3. HER家族磷酸化及PI3K结合检测：用吉非替尼盐酸盐（Gefitinib hydrochloride）处理HER2过表达肿瘤细胞，制备细胞裂解液。通过免疫印迹检测EGFR、HER2、HER3的磷酸化水平；采用免疫共沉淀（co-IP）检测HER3与PI3K的结合情况。分析磷酸化水平及蛋白-蛋白相互作用的变化，评估化合物对HER家族信号通路的抑制效果[3]

目的：EGF受体（EGFR）酪氨酸激酶抑制剂（TKI）已被发现对肺癌癌症有效，但随着其使用的增加，对这些药物的临床耐药性已经发展。二甲双胍是一种广泛使用的抗糖尿病药物，在几种癌症模型中也表现出显著的生长抑制和促凋亡作用，无论是单独使用还是与化疗药物联合使用<小时> 实验设计：通过MTT、溴化物分析、流式细胞术、凤尾藻非依赖性生长、免疫共沉淀和蛋白质印迹分析，评估吉非替尼、选择性EGFR-TKI和二甲双胍对一组非小细胞肺癌（NSCLC）细胞系的影响<小时> 结果：二甲双胍与吉非替尼的联合用药在携带野生型LKB1基因的NSCLC细胞系中诱导了强烈的抗增殖和促凋亡作用。然而，用二甲双胍作为单一药物治疗，通过增加C-RAF/B-RAF异二聚作用诱导丝裂原活化蛋白激酶（MAPK）的活化和磷酸化。在二甲双胍治疗中加入吉非替尼对EGFR磷酸化和下游信号传导的抑制消除了这一现象，并在体外和体内诱导了强烈的凋亡作用<小时> 结论：二甲双胍和吉非替尼对LKB1野生型NSCLC细胞具有协同作用。然而，还需要进一步的研究来更好地研究二甲双胍作用对RAS/RAF/MAPK途径的影响，以及二甲双胍与分子靶向药物联合使用的最佳情况。[4]

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1. 细胞增殖检测（EGFR依赖型细胞）：将对EGF敏感的肿瘤细胞接种于96孔板，过夜培养。加入系列稀释的吉非替尼盐酸盐（Gefitinib hydrochloride），在标准培养条件下孵育72小时。采用比色试剂（如MTT或溴化物法）检测细胞活力，从剂量-反应曲线计算抑制细胞增殖的EC₅₀/IC₅₀值[1]
2. 锚定非依赖性生长检测：将NR6（对照）、NR6wtEGFR、NR6W（高EGFR）、NR6M（EGFRvIII）细胞用0-2μM 吉非替尼盐酸盐（Gefitinib hydrochloride）处理后接种于软琼脂中；NR6wtEGFR和NR6W细胞分别用10nM和0.1nM EGF刺激。培养18天后计数克隆，以未处理组克隆数为基准计算克隆数百分比，评估化合物对锚定非依赖性生长的影响[2]
3. 下游信号免疫印迹检测：将细胞（如NSCLC细胞、HER2过表达细胞）用吉非替尼盐酸盐（Gefitinib hydrochloride）处理（联合用药研究中需先预处理二甲双胍）。细胞裂解液经SDS-PAGE分离后转移至膜上，用针对磷酸化和总下游信号分子（ERK、AKT、PLC-γ、STAT3）的抗体进行检测。对条带强度定量，分析化合物对信号通路激活的影响[3,4]
4. 凋亡检测（联合治疗）：将LKB1野生型NSCLC细胞分别用吉非替尼盐酸盐（Gefitinib hydrochloride）单独处理、二甲双胍单独处理或二者联合处理。通过流式细胞术（Annexin V/PI染色）或免疫印迹（检测剪切型caspase-3或PARP）检测凋亡；比较各组凋亡细胞百分比或凋亡标志物水平，评估协同促凋亡效应[4]
5. 肺成纤维细胞增殖检测：从辐射损伤大鼠中分离肺成纤维细胞，用吉非替尼盐酸盐（Gefitinib hydrochloride）处理。采用细胞计数试剂盒或BrdU掺入法检测细胞增殖；通过免疫印迹检测成纤维细胞中EGFR表达，评估化合物对成纤维细胞功能的影响[5]

Dissolved in 0.5% polysorbate; 100 mg/kg; Oral gavage
Nude mice (cba nu/nu) are intra-dermal injected with LoVo cells. Background: Gefitinib, an inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, has been reported to be associated with interstitial lung disorders, and their high incidence and mortality have become a matter of great concern, especially in Japan. In this study, we investigated the effect of gefitinib on different phases of radiation-induced lung disorders in an experimental model. Methods: The thoraxes of Wistar rats were irradiated on day 1 with a single X-ray dose of 20 Gy, and gefitinib (50 mg/kg/day) was orally administered from day 1 to 14. The rat lungs were harvested on days 15 and 57 and the bronchoalveolar lavage (BAL) was performed.[5]

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1. Tumor xenograft model (efficacy study): Female nude mice are subcutaneously implanted with human tumor cells (e.g., A431, HER2-overexpressing breast cancer cells, NSCLC cells). When tumors reach a mean volume of ~100-150 mm³, mice are randomized into treatment and control groups. Gefitinib hydrochloride (Gefitinib) is dissolved in a suitable vehicle (e.g., aqueous solution or appropriate organic solvent mixture) and administered orally by gavage once daily at doses of 3.125-200 mg/kg. Tumor volume and body weight are measured twice weekly for 2-4 weeks (or >3 months for long-term studies); tumor growth inhibition (TGI) is calculated relative to the vehicle control [1]
2. Radiation-induced lung injury model: Male Wistar rats receive a single 20 Gy X-ray irradiation to the thorax on day 1. Gefitinib hydrochloride (Gefitinib) is administered orally at 50 mg/kg/day from day 1 to 14. Rats are euthanized on day 15 and 57; bronchoalveolar lavage (BAL) is performed to collect inflammatory cells, and lung tissues are harvested for histopathological analysis (inflammatory cell infiltration, collagen content) and detection of pro-inflammatory cytokines (IL-6, IL-1β) [5]
3. Combination therapy xenograft model: Nude mice bearing LKB1 wild-type NSCLC xenografts are randomized into four groups: vehicle control, Gefitinib hydrochloride (Gefitinib) alone (oral gavage, dose based on previous efficacy studies), metformin alone (oral administration), and combination of both agents. Drug administration is continued for a set period; tumor burden is measured regularly, and tumor growth curves are generated to assess synergistic effects [4]

Gefitinib hydrochloride (gefitinib) has shown good oral bioavailability in preclinical studies, supporting its once-daily oral dosing regimen; however, detailed data on its half-life, absorption, distribution, metabolism or excretion (e.g., clearance, volume of distribution) are not provided in the relevant literature [1].

1. In nude mice, long-term (>3 months) administration of effective tumor-inhibiting doses of gefitinib hydrochloride (gefitinib) was well tolerated; no significant treatment-related toxicities (e.g., weight loss, organ damage) were observed.[1] 2. In Wistar rats treated with gefitinib hydrochloride (gefitinib) (50 mg/kg/day, orally, 1–14 days) after chest irradiation: it exacerbated radiation-induced pneumonia (increased inflammatory cell infiltration and pro-inflammatory cytokines IL-6/IL-1β in the lungs on day 15), but reduced radiation-induced pulmonary fibrosis (decreased lung collagen content and inhibited lung fibroblast proliferation on day 57).[5]

[1]. ZD1839 (Iressa): an orally active inhibitor of epidermal growth factor signaling with potential for cancer therapy. Cancer Res. 2002 Oct 15;62(20):5749-54.

[2]. Differential response to gefitinib of cells expressing normal EGFR and the mutant EGFRvIII. Br J Cancer. 2005 Oct 17;93(8):915-23.

[3]. The tyrosine kinase inhibitor ZD1839 ("Iressa") inhibits HER2-driven signaling and suppresses the growth of HER2-overexpressing tumor cells. Cancer Res. 2001 Oct 1;61(19):7184-8.

[4]. Synergistic effects of metformin treatment in combination with gefitinib, a selective EGFR tyrosine kinase inhibitor, in LKB1 wild-type NSCLC cell lines. Clin Cancer Res. 2013 Jul 1;19(13):3508-19.

[5]. Epidermal growth factor receptor-tyrosine kinase inhibitor (gefitinib) augments pneumonitis, but attenuates lung fibrosis in response to radiation injury in rats. J Med Invest. 2012;59(1-2):174-85.

Epidermal growth factor receptor (EGFR) has become a promising target for anticancer therapy due to its important role in tumor growth, metastasis, angiogenesis, and tumor resistance to chemotherapy and radiotherapy. We developed a low molecular weight EGFR tyrosine kinase inhibitor (EGFR-TKI) ZD1839 (Iressa(2)). ZD1839 is a substituted aniline quinazoline compound and a potent EGFR-TKI (IC50 = 0.033 μM) that selectively inhibits EGF-stimulated tumor cell growth (IC50 = 0.054 μM) and blocks EGFR autophosphorylation in EGF-stimulated tumor cells. In mouse models carrying multiple human xenograft tumors, once-daily oral administration of ZD1839 dose-dependently inhibited tumor growth. EGFR expression levels did not determine the sensitivity of xenograft tumors to ZD1839. Long-term (>3 months) ZD1839 treatment was well tolerated in mice carrying A431 xenograft tumors. ZD1839 completely inhibited tumor growth and induced regression of established tumors. No drug-resistant tumors developed during ZD1839 treatment, but some tumors relapsed after discontinuation of the drug. These studies suggest that ZD1839 has potential applications in treating various human tumors and indicate that once-daily oral administration may be a suitable treatment regimen. [1]

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1. Gefitinib hydrochloride (gefitinib) is a low molecular weight, orally effective aniline quinazoline derivative and the first selective EGFR tyrosine kinase inhibitor (EGFR-TKI) for cancer treatment; it exerts its antitumor effect by inhibiting EGFR-mediated signal transduction, which is crucial for tumor growth, metastasis, angiogenesis, and resistance to chemotherapy/radiotherapy [1]
2. The sensitivity of tumor cells to gefitinib hydrochloride (gefitinib) is not entirely determined by the level of EGFR expression; factors such as EGFR mutations (e.g., EGFRvIII) and HER2 overexpression also affect efficacy: tumors with HER2 overexpression are particularly sensitive, while cells expressing EGFRvIII show a biphasic response (low-dose stimulation, high-dose inhibition) [2,3]
3. The synergistic effect of gefitinib and metformin is specifically targeted at the LKB1 wild-type non-small cell lung cancer (NSCLC) cell line, because metformin alone can activate the MAPK pathway in these cells, while gefitinib can block this non-targeted activation, thereby enhancing the anti-tumor efficacy [4]. Gefitinib has a dual effect on radiation-induced lung injury: it exacerbates the inflammatory phase (pneumonia) but can also alleviate the fibrotic phase, suggesting that there may be risks and benefits when used in combination with thoracic radiotherapy [5].

C22H24N4O3FCL.HCL

483.3633

482.128

184475-55-6

Gefitinib;184475-35-2

19077490

Typically exists as white to off-white solids at room temperature

607.7ºC at 760 mmHg

321.3ºC

4.9E-15mmHg at 25°C

5.088

68.74

2

8

8

32

545

0

ClC1=C(C=CC(NC2=NC=NC3=C2C=C(C(OC)=C3)OCCCN4CCOCC4)=C1)F.[H]Cl

QUINXWLATMJDQF-UHFFFAOYSA-N

InChI=1S/C22H24ClFN4O3.ClH/c1-29-20-13-19-16(12-21(20)31-8-2-5-28-6-9-30-10-7-28)22(26-14-25-19)27-15-3-4-18(24)17(23)11-15;/h3-4,11-14H,2,5-10H2,1H3,(H,25,26,27);1H

N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-morpholin-4-ylpropoxy)quinazolin-4-amine;hydrochloride

ZD1839 HCl; ZD 1839 HCl; ZD-1839 HCl; Gefitinib HCl; trade name: Iressa.Gefitinib hydrochloride; 184475-55-6; gefitinib hcl; Gefitinib (hydrochloride); ZD-1839 hydrochloride; Gefitinib hydrochloride salt; N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-morpholin-4-ylpropoxy)quinazolin-4-amine;hydrochloride; 4-Quinazolinamine,N-(3-chloro-4-fluorophenyl)-7-methoxy-6-[3-(4-morpholinyl)propoxy]-,monohydrochloride;

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)

5% DMSO+corn oil: 2.5 mg/mL

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。