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Efficacy(The capacity for beneficial change (or therapeutic effect) of a given intervention) in combination with a broad range of standard therapies

Combining anticancer agents with different MoA may lead to increased efficacy through additive, and even synergistic, effects

  • The precise nature of VEGF(A protein that promotes angiogenesis and is known to be a prognostic factor in several types of tumour) inhibition by Avastin makes this agent an ideal partner for combination with approaches aimed at other mechanisms of tumour(An abnormal growth of cells, forming a mass of tissue) proliferation(The reproduction of cells by multiplication of parts).1,2

Additional benefit may be gained through normalisation of tumour vasculature by Avastin, which reduces interstitial pressure(Fluid pressure pertaining to parts or interspaces of a tissue) and increases the delivery of other agents to the tumour. 3,4

This section provides an overview of the clinical efficacy of Avastin in combination with different types of anticancer agent.

Combining Avastin with conventional chemotherapy leads to superior efficacy

The specific chemotherapy agents used in clinical practice vary considerably between tumour types; trials have investigated Avastin in combination with the most frequently used regimens in each indication.

Avastin has demonstrated efficacy in phase III trials when combined with a variety of chemotherapy agents and regimens

  • mCRC: IFL, XELOX, FOLFOX4.5,6
  • NSCLC: carboplatin/paclitaxel, cisplatin/gemcitabine.7,8
  • mBC: paclitaxel.9

Large safety studies have explored further combinations in mCRC and NSCLC.10–12

Avastin in combination with other standard anticancer agents and treatment modalities

The ability to apply direct and continuous VEGF inhibition with Avastin in combination with other treatment modalities may increase the available therapeutic options in a number of tumour types.

In addition to chemotherapy, other types of systemic therapy used in the treatment of cancer include

  • Immunotherapy.
  • Endocrine therapy
  • Targeted agents (those acting via recognition of a specific tumour cell marker, e.g. trastuzumab for HER-2).

Immunotherapy is commonly used in the treatment of RCC

  • In a phase III trial, Avastin significantly increased PFS(The time from trial entry to disease progression or death from any cause) (p<0.0001) and ORR(The proportion of patients with defined tumour shrinkage; generally the sum of partial responses plus complete responses) (p<0.0001) in combination with IFN-α compared with IFN-α plus placebo (figure).13

Endocrine therapies, such as aromatase inhibitors, and the targeted agent trastuzumab are each used to treat specific subgroups of patients with mBC

  • Ongoing phase III studies are investigating Avastin in combination with these treatment modalities.

Summary

In clinical trials, Avastin has proven efficacy in combination with a broad range of standard anticancer therapies, including cytotoxic(Refers to an agent that acts by causing the death of cells in the body, thus causing a reduction in cell numbers) chemotherapy and immunotherapy.

References

  1. Gerber HP, Ferrara N. Cancer Res 2005;65:671–80.
  2. Kerbel RS. Science 2006;312:1171–5.
  3. Jain RK. Science 2005;307:58–62.
  4. Jain RK. Nat Med 2001;7:987–9.
  5. Hurwitz H, Fehrenbacher L, Novotny W, et al. N Engl J Med 2004;350:2335–42.
  6. Saltz L, Clarke S, Díaz-Rubio E, et al. J Clin Oncol 2008;26:2013–9.
  7. Sandler A, Gray R, Perry MC, et al. N Engl J Med 2006;355:2542–50.
  8. Reck M, von Pawel J, Zatloukal P, et al. J Clin Oncol 2009;27:1227–34.
  9. Gray R, Bhattacharya S, Bowden C, Miller K, Comis RL. J Clin Oncol 2009;27:4966–72.
  10. Kozloff M, Hainsworth J, Badarinath S, et al. Presented at: 2007 Gastrointestinal Cancers Symposium; 19–21 January 2007; Orlando Fl. Abstract 375; poster presentation. Available at: http://www.asco.org.
  11. Van Cutsem E, Rivera F, Berry S, et al. Ann Oncol 2009;20:1842–7.
  12. Wu Y, Jiang G, Reck M, et al. Proceedings of the International Union Against Cancer (UICC), Geneva, Switzerland August 2008;POS-B174.
  13. Escudier B, Pluzanska A, Koralewski P, et al. Lancet 2007;370:2103–11.

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