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曲妥珠-單抗

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  • 公司名稱(chēng)杭州昊鑫生物科技股份有限公司
  • 品       牌MCE
  • 型       號(hào)HY-P9907
  • 所  在  地杭州市
  • 廠(chǎng)商性質(zhì)代理商
  • 更新時(shí)間2024/6/27 17:02:15
  • 訪(fǎng)問(wèn)次數(shù)454
產(chǎn)品標(biāo)簽:

Trastuzumab

規(guī)格
1mg1600.00元10000 支可售
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杭州昊鑫生物科技股份有限公司成立于2009年初,是一家面向生命科學(xué)領(lǐng)域,從事科研機(jī)構(gòu)、高校、院所及生產(chǎn)企業(yè)所需科研試劑、耗材,儀器銷(xiāo)售和服務(wù)面向全國(guó)。

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胎牛血清、MCE抑制劑激動(dòng)劑、RNA提取試劑盒、ELISA試劑盒、重組蛋白
CAS號(hào) 180288-69-1 產(chǎn)地 國(guó)產(chǎn)
規(guī)格 1mg 級(jí)別 化工級(jí)
證書(shū) ISO系列證書(shū)
Trastuzumab 是一種人源化 IgG1 單克隆抗體,其以高親和力與 HER2 選擇性結(jié)合。Trastuzumab 可用于 HER2 陽(yáng)性轉(zhuǎn)移性乳腺癌和 HER2 陽(yáng)性胃癌的研究。
曲妥珠-單抗 產(chǎn)品信息

Trastuzumab (Synonyms: 曲妥珠-單抗; Anti-Human HER2, Humanized Antibody)

Trastuzumab 是一種人源化 IgG1 單克隆抗體,其以高親和力與 HER2 選擇性結(jié)合。Trastuzumab 可用于 HER2 陽(yáng)性轉(zhuǎn)移性乳腺癌和 HER2 陽(yáng)性胃癌 的研究。

生物活性

Trastuzumab is a humanized IgG1 monoclonal antibody for patients with invasive breast cancers that overexpress HER2. Trastuzumab has the potential for HER2 Positive Metastatic Breast Cancer and HER2 Positive Gastric Cancer research.


IC50 & Target[1]

HER2


體外研究(In Vitro)

Treatment of HER2-overexpressing breast cancer cell lines with Trastuzumab results in induction of p27KIP1 and the Rb-related protein, p130, which in turn significantly reduces the number of cells undergoing S-phase. A number of other phenotypic changes are observed in vitro as a consequence of Trastuzumab binding to HER2-overexpressing cells. Interaction of Trastuzumab with the human immune system via its human immunoglobulin G1 Fc domain may potentiate its antitumor activities. in vitro studies demonstrate that Trastuzumab is very effective in mediating antibody-dependent cell-mediated cytotoxicity against HER2-overexpressing tumor targets[1]. Trastuzumab consists of two antigen-specific sites that bind to the juxtamembrane portion of the extracellular domain of the HER2 receptor and that prevent the activation of its intracellular tyrosine kinase. Trastuzumab recruits immune effector cells that are responsible for antibody-dependent cytotoxicity[2]. The presence of Trastuzumab IgG significantly increases killing of all breast cancer cell lines. The ADCC activity of PBMCs evoked by Trastuzumab is equally strong against Trastuzumab-sensitive (SKBR-3) or Trastuzumab-resistant (JIMT-1) breast cancer cells, with dose-dependent cell death reaching 50–60% killing at an effector/target ratio of 60:1[3].


體內(nèi)研究(In Vivo)

Trastuzumab treatment of mouse xenograft models results in marked suppression of tumor growth. When given in combination with standard cytotoxic chemotherapeutic agents, Trastuzumab treatment generally results in statistically superior antitumor efficacy compared with either agent given alone[1]. Trastuzumab causes a significant growth inhibition of the outgrowth of macroscopic JIMT-1 xenograft tumors in both nude and SCID mice[3].


Clinical Trial

NCT NumberSponsorConditionStart DatePhase
NCT04158258Hoffmann-La Roche|Latin American Cooperative Oncology Group
Breast Cancer
February 21, 2020
NCT02774681Northwestern University|Pfizer|National Cancer Institute (NCI)
Breast Carcinoma Metastatic in the Brain|Estrogen Receptor Negative|HER2+Neu Negative|HER2+Neu Positive|Progesterone Receptor Negative|Recurrent Breast Carcinoma|Stage IV Breast Cancer
August 31, 2016Phase 2
NCT03493854Hoffmann-La Roche
Early Breast Cancer
June 14, 2018Phase 3


分子量:145531.50


Formula:C6470H10012N1726O2013S42


CAS 號(hào):180288-69-1


中文名稱(chēng):曲妥珠-單抗;曲妥-單抗;群司珠-單抗


儲(chǔ)存方式;Please store the product under the recommended conditions in the Certificate of Analysis.


參考文獻(xiàn)

  • [1]. Sliwkowski MX, et al. Nonclinical studies addressing the mechanism of action of trastuzumab. Semin Oncol. 1999 Aug;26(4 Suppl 12):60-70.

    [2]. Hudis CA, et al. Trastuzumab--mechanism of action and use in clinical practice. N Engl J Med. 2007 Jul 5;357(1):39-51.

    [3]. Barok M, et al. Trastuzumab causes antibody-dependent cellular cytotoxicity-mediated growth inhibition of submacroscopic JIMT-1 breast cancer xenografts despite intrinsic drug resistance. Mol Cancer Ther. 2007 Jul;6(7):2065-72.









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