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Axitinib

chemical compound

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Record originEnglish Wikipedia
Text licenseCC BY-SA 4.0
Source revisionJan 29, 2026
Entity authorityQ4830631
Source-derived summary

Axitinib, sold under the brand name Inlyta, is a small molecule tyrosine kinase inhibitor developed by Pfizer. It has been shown to significantly inhibit growth of breast cancer in animal (xenograft) models and has shown partial responses in clinical trials with renal cell carcinoma (RCC) and several other tumour types.

It was approved to treat renal cell carcinoma by the U.S. Food and Drug Administration after showing a modest increase in progression-free survival, though there have been reports of fatal adverse effects.

Medical uses

Renal cell carcinoma

It has received approval for use as a treatment for renal cell carcinoma from the US Food and Drug Administration (FDA) (January 2012), the European Medicines Agency (EMA) (September 2012), the UK Medicines and Healthcare products Regulatory Agency (MHRA) (September 2012) and the Australian Therapeutic Goods Administration (TGA) (July 2012).

Clinical trials

A Phase II clinical trial showed good response in combination chemotherapy with gemcitabine for advanced pancreatic cancer. However, Pfizer reported on 30 January 2009, that Phase III clinical trials of the drug when used in combination with gemcitabine showed no evidence of improved survival rates over treatments using gemcitabine alone for advanced pancreatic cancer and halted the trial.

In 2010, a Phase III trial for previously treated metastatic renal cell carcinoma (mRCC) showed significantly extended progression-free survival when compared to sorafenib. In December 2011, the Oncologic Drugs Advisory Committee (ODAC) voted unanimously to recommend that US FDA approve axitinib for the second-line treatment of patients with advanced renal cell carcinoma (RCC), based on the results of the Phase III trial comparing axitinib and sorafenib.

It has also been studied in combination with the ALK1 inhibitor dalantercept.

A study published in 2015 showed that axitinib effectively inhibits a mutated gene (BCR-ABL1[T315I]) that is common in chronic myeloid leukemias and adult acute lymphoblastic leukemias which have become resistant to other tyrosine kinase inhibitors like imatinib.

Editorial summary

Begin with the source’s own compact description: “Axitinib” is chemical compound. The dossier treats that line as a proposition to test through Axitinib, chemical and compound, not as a finished interpretation.

Editorial reviewUseful for establishing the present vocabulary of the subject while preserving a route back to the evidence on which that vocabulary rests. The current lead gives the account dated anchors—2012, 2009, 2010, 2011—that can be checked directly. The selected authority fields contribute no independent date. For this dossier, Axitinib, chemical and compound is the immediate research focus.
Editorial analysis

Why this record matters

The phrase “chemical compound” supplies a clear boundary for inquiry. It also exposes the unanswered questions: who defined that boundary, when it became stable and which sources sit outside it.

Evidence profile

The date and method of observation matter as much as the stated conclusion, especially where classification or consensus has changed. The source revision retrieved here is dated Jan 29, 2026. The linked authority identifier is Q4830631. None of the 0 selected statements returned an explicit reference. The first chronological checks are 2012, 2009, 2010 and 2011.

Critical limits

Current terminology should not be projected backward without checking the classification used when the underlying evidence was created. The source lead contains qualifying language; that uncertainty should survive quotation, summary and reuse. Authority statements aid reconciliation but still require their own references, qualifiers and ranks to be checked.

How to read it

Check terminology, classification and the date of the cited evidence. Scientific names and technical consensus can change while older records retain historical value.

Best used for
  • Current terminology
  • Classification context
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  1. Establish the record: confirm the title “Axitinib”, its source revision and the description used here.
  2. Expand the search: follow Axitinib primary sources, Axitinib archive and Axitinib research across catalogues and specialist indexes.
  3. Test the account: compare the strongest cited source with the responsible institution’s current record and note any disagreement.

Questions for further research

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Source & attribution

This entry incorporates text from Axitinib” on English Wikipedia. Contributors are listed in the page history. Text is available under the Creative Commons Attribution-ShareAlike 4.0 License. Selected authority identifiers and statements are retrieved from Wikidata under CC0; their references and qualifiers remain part of the verification path.