Trastuzumab - CAS 180288-69-1
Catalog number: B0084-061382
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
Molecular Weight:
Trastuzumab is a monoclonal antibody drug for the treatment of breast cancer which is HER2 receptor positive. It acts via binding to HER2 receptor to suppress cell duplication.
Brife Description:
monoclonal antibody, breast cancer, HER2 receptor
Light chain (1 and 2):
Heavy chain (1 and 2)
Herceptin; RhuMab HER2; Anti HER2, Ig gamma-1 chain C region; Recombinant humanized anti-HER2 antibody; IMMunoglobulin G1,anti-(huMan p185neu receptor) (huMan-Mouse Monoclonal rhuMab HER2 g1-chain), disulfide with huMan-MouseMonoclonal rhuMab HER2 light chain, diMer
the treatment of HER2 receptor positive breast cancer
Shelf Life:
2 years
Canonical SMILES:
1.miR-155 downregulates ErbB2 and suppresses ErbB2-induced malignant transformation of breast epithelial cells.
He XH1,2, Zhu W3, Yuan P1,2, Jiang S1,2, Li D4, Zhang HW3, Liu MF1,2,5. Oncogene. 2016 Apr 11. doi: 10.1038/onc.2016.132. [Epub ahead of print]
ErbB2 is a vital breast cancer gene and its overexpression has a decisive role in breast tumor initiation and malignant progression. However, the molecular mechanisms that underlie ErbB2 dysregulation in breast cancer cells remain incompletely understood. In this study, we found that ErbB2 expression is inversely correlated with the level of miR-155, a well-documented oncogenic miRNA, in ErbB2-positive breast tumors. We further determined that miR-155 potently suppresses ErbB2 in breast cancer cells. Mechanistically, miR-155 acts to downregulate ErbB2 via two distinct mechanisms. First, miR-155 represses ErbB2 transcription by targeting HDAC2, a transcriptional activator of ErbB2. Second, miR-155 directly targets ErbB2 via a regulatory element in its coding region. Intriguingly, miR-155 is upregulated by trastuzumab and in turn leads to a reduction of ErbB2 expression in trastuzumab-treated ErbB2-positive breast cancer cells. Functional studies showed that miR-155 inhibits ErbB2-induced malignant transformation of human breast epithelial cells.
2.Neratinib Plus Paclitaxel vs Trastuzumab Plus Paclitaxel in Previously Untreated Metastatic ERBB2-Positive Breast Cancer: The NEfERT-T Randomized Clinical Trial.
Awada A1, Colomer R2, Inoue K3, Bondarenko I4, Badwe RA5, Demetriou G6, Lee SC7, Mehta AO8, Kim SB9, Bachelot T10, Goswami C11, Deo S12, Bose R13, Wong A14, Xu F14, Yao B14, Bryce R14, Carey LA15. JAMA Oncol. 2016 Apr 14. doi: 10.1001/jamaoncol.2016.0237. [Epub ahead of print]
Importance: Efficacious ERBB2 (formerly HER2 or HER2/neu)-directed treatments, in addition to trastuzumab and lapatinib, are needed.
3.Where did the linker-payload go? - A quantitative investigation on the destination of the released linker-payload from an antibody-drug conjugate with a maleimide linker in plasma.
Wei C, Zhang G, Clark T, Barletta F, Tumey LN, Rago B, Hansel S, Han X. Anal Chem. 2016 Apr 13. [Epub ahead of print]
The reactive thiol of cysteine is often used for coupling maleimide-containing linker-payloads to antibodies resulting in the generation of antibody drug conjugates (ADCs). Currently, a numbers of ADCs in drug development are made by coupling a linker-payload to native or engineered cysteine residues on the antibody. An ADC conjugated via hinge-cysteines to an auristatin payload was used as a model in this study to understand the impact of the maleimide linkers on ADC stability. The payload was conjugated to trastuzumab by a protease-cleavable linker, maleimido-caproyl-valine-citruline-p-amino-benzyloxy carbonyl (mcVC-PABC). In plasma stability assays, when the ADC (Trastuzumab-mcVC-PABC-Auristatin-0101) was incubated with plasma over a 144-hour (h) time-course, a discrepancy was observed between the measured released free payload concentration and the measured loss of drug-to-antibody ratio (DAR), as measured by LC-MS. We found that an enzymatic release of payload from ADC-depleted human plasma at 144h was able to account for almost 100% of the DAR loss.
4.Effect of neoadjuvant chemotherapy on breast cancer phenotype, ER/PR and HER2 expression - Implications for the practising oncologist.
Gahlaut R1, Bennett A1, Fatayer H2, Dall BJ3, Sharma N3, Velikova G4, Perren T5, Dodwell D4, Lansdown M2, Shaaban AM6. Eur J Cancer. 2016 Apr 7;60:40-48. doi: 10.1016/j.ejca.2016.03.006. [Epub ahead of print]
PURPOSE: To assess the effect of neoadjuvant chemotherapy (NACT) on breast cancer characteristics, hormone receptors and human epidermal growth factor receptor 2 (HER2) expression and whether testing should be repeated on residual tumours.
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