Gap Inc V.GAP

testing timeline example

[uneven]

Here is the timeline for Imatinib (Gleevec) as an example...

https://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1934577

Brian Druker, a physician scientist and fellow contributor to this Review Series, had been working on CML since the early 1990s, and once he set up his own group at Oregon Health & Science University in Portland in 1993 and started treating CML patients, he became determined to find a better treatment for this disease. The logical approach was to develop a small molecule inhibitor of the BCR-ABL tyrosine kinase activity, since this would be expected to block the growth of the transformed cells. To try to find a suitable inhibitory compound, he collaborated with the members of the tyrosine kinase inhibitor program at CIBA-Geigy. Working closely with Lydon, Buchdunger, and Zimmermann, Druker identified CGP57148B as a potent and relatively selective v-Abl inhibitor. Together with Buchdunger, Druker showed that CGP57148B was able to inhibit the growth of CML cells and BCR-ABL–transformed cells both in culture and when grown as tumors in mice (92, 93). There was little evidence of toxicity in mice, and, emboldened by these results, in June 1998 Druker and Charles Sawyers initiated a phase I/II clinical trial in chronic phase CML patients resistant to prior interferon therapy (94). This trial, and subsequent large-scale follow-up phase II clinical trials, showed that imatinib was very effective in treating chronic phase CML and had palliative, but usually not long-lasting, effects in the acute blast crisis phase (95, 96) that were commonly due to the development of resistance mutations in BCR-ABL itself. These successes led to an accelerated approval process by the FDA, and imatinib was approved for the treatment of CML on May 10, 2001.