Imatinib

From The School of Biomedical Sciences Wiki
(Difference between revisions)
Jump to: navigation, search
 
Line 1: Line 1:
<u>'''Introduction'''</u><br>Imatinib (“Gleevec” or “Glivec”), is a 2-phenyl amino pyrimidine derivative. It can be classified as tyrosine kinase [[Enzyme Inhibitors|inhibitor]] (TKI) <ref name="(1)">Cancer Research UK, Imatinib(Glivec) [Available at]:https://www.cancerresearchuk.org/about-cancer/cancer-in-general/treatment/cancer-drugs/drugs/imatinib</ref> .This protein has revolutionized the treatment of [[Chronic myeloid leukimia|chronic myeloid leukemia ]](CML) in 2001.  
+
Imatinib (“Gleevec” or “Glivec”), is a 2-phenyl amino pyrimidine derivative. It can be classified as tyrosine kinase [[Enzyme Inhibitors|inhibitor]] (TKI)<ref name="(1)">Cancer Research UK, Imatinib(Glivec) [Available at]:https://www.cancerresearchuk.org/about-cancer/cancer-in-general/treatment/cancer-drugs/drugs/imatinib</ref>. This protein has revolutionized the treatment of [[Chronic myeloid leukimia|chronic myeloid leukemia ]](CML) in 2001.  
  
<br>'''<u>Clinical Pharmacology&nbsp;</u>'''<br>The [[Active site|active sites of]] tyrosine kinases each have a binding site for [[ATP|ATP.]] The catalysed enzymatic activity, known as protein tyrosine [[Phosphorylation|phosphorylation]] is the transfer of a terminal phosphate from ATP to tyrosine residues on its substrates.&nbsp;Deregulation of tyrosine kinase activity has been shown to play a central role in the pathogenesis of human cancers.&nbsp;
+
=== Clinical Pharmacology ===
  
<br>Imatinib works by binding close to the ATP binding site, locking it in a closed conformation, therefore inhibiting the enzyme activity of the protein semicompetitively. This process ultimately prevents the occurance of downstream signaling pathways which promote leukemogenesis.<ref name="(2)">Iqbal, N., &amp;amp;amp; Iqbal, N. (2014). Imatinib: a breakthrough of targeted therapy in cancer. Chemotherapy research and practice, 2014.[Available at]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055302/</ref><br>''<br>'''''<u>Clinical implications&nbsp;:</u>&nbsp;''''''<br>'''This medication is used to treat certain types of cancer such as chronic myeloid leukemia (CML) by Inhibiting at BCR-ABL gene on chromosome 22 (Philadelphia chromosome)<ref>Kang, Z. J., Liu, Y. F., Xu, L. Z., Long, Z. J., Huang, D., Yang, Y., Liu, B., Feng, J. X., Pan, Y. J., Yan, J. S., … Liu, Q. (2016). The Philadelphia chromosome in leukemogenesis. Chinese journal of cancer, 35, 48. doi:10.1186/s40880-016-0108-0. [Available at]:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896164/</ref>. It is a chemotherapy drug that works by slowing or stopping the growth of cancer cells.<br>
+
The active sites of [[tyrosine kinase|tyrosine kinases]] each have a binding site for [[ATP|ATP.]] The catalysed enzymatic activity, known as protein tyrosine [[Phosphorylation|phosphorylation]] is the transfer of a terminal [[phosphate|phosphate]] from ATP to [[tyrosine|tyrosine]] residues on its substrates. Deregulation of tyrosine kinase activity has been shown to play a central role in the pathogenesis of human cancers.  
  
= <br>'''References&nbsp;:'''  =
+
Imatinib works by binding close to the ATP binding site, locking it in a closed conformation, therefore inhibiting the enzyme activity of the protein semi-competitively. This process ultimately prevents the occurrence of downstream signaling pathways which promote leukemogenesis<ref name="(2)">Iqbal, N., &amp;amp;amp;amp;amp; Iqbal, N. (2014). Imatinib: a breakthrough of targeted therapy in cancer. Chemotherapy research and practice, 2014.[Available at]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055302/</ref>.
  
<references />'''<br><br>'''
+
=== Clinical implications  ===
 +
 
 +
This medication is used to treat certain types of cancer such as [[chronic myeloid leukaemia|chronic myeloid leukaemia]] (CML) by Inhibiting at [[BCR-ABL gene|BCR-ABL]] [[gene|gene]] on [[chromosome 22|chromosome 22]] (Philadelphia chromosome)<ref>Kang, Z. J., Liu, Y. F., Xu, L. Z., Long, Z. J., Huang, D., Yang, Y., Liu, B., Feng, J. X., Pan, Y. J., Yan, J. S., … Liu, Q. (2016). The Philadelphia chromosome in leukemogenesis. Chinese journal of cancer, 35, 48. doi:10.1186/s40880-016-0108-0. [Available at]:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896164/</ref>. It is a chemotherapy drug that works by slowing or stopping the growth of cancer cells.
 +
 
 +
=== References  ===
 +
 
 +
<references />

Latest revision as of 21:03, 6 December 2018

Imatinib (“Gleevec” or “Glivec”), is a 2-phenyl amino pyrimidine derivative. It can be classified as tyrosine kinase inhibitor (TKI)[1]. This protein has revolutionized the treatment of chronic myeloid leukemia (CML) in 2001.

Clinical Pharmacology

The active sites of tyrosine kinases each have a binding site for ATP. The catalysed enzymatic activity, known as protein tyrosine phosphorylation is the transfer of a terminal phosphate from ATP to tyrosine residues on its substrates. Deregulation of tyrosine kinase activity has been shown to play a central role in the pathogenesis of human cancers.

Imatinib works by binding close to the ATP binding site, locking it in a closed conformation, therefore inhibiting the enzyme activity of the protein semi-competitively. This process ultimately prevents the occurrence of downstream signaling pathways which promote leukemogenesis[2].

Clinical implications

This medication is used to treat certain types of cancer such as chronic myeloid leukaemia (CML) by Inhibiting at BCR-ABL gene on chromosome 22 (Philadelphia chromosome)[3]. It is a chemotherapy drug that works by slowing or stopping the growth of cancer cells.

References

  1. Cancer Research UK, Imatinib(Glivec) [Available at]:https://www.cancerresearchuk.org/about-cancer/cancer-in-general/treatment/cancer-drugs/drugs/imatinib
  2. Iqbal, N., &amp;amp;amp;amp; Iqbal, N. (2014). Imatinib: a breakthrough of targeted therapy in cancer. Chemotherapy research and practice, 2014.[Available at]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055302/
  3. Kang, Z. J., Liu, Y. F., Xu, L. Z., Long, Z. J., Huang, D., Yang, Y., Liu, B., Feng, J. X., Pan, Y. J., Yan, J. S., … Liu, Q. (2016). The Philadelphia chromosome in leukemogenesis. Chinese journal of cancer, 35, 48. doi:10.1186/s40880-016-0108-0. [Available at]:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896164/
Personal tools
Namespaces
Variants
Actions
Navigation
Toolbox