Tipranavir: Difference between revisions

Line 6:

* Date of FDA Approval (Patent Expiration): 2005 (2015) <br />

* 2009 Sales: $200 Million

* Importance: At the ~~time of its approval, it was far more powerful than prior antiretroviral drugs. Has subsequently been largely replaced with newer drugs which are less likely to promote resistance, such as~~ [[~~Lopinavir~~]] and ~~[[Atazanavir]]~~

* Importance: It was the ninth [[HIV Protease]] inhibitor approved by the FDA for treatment of HIV. It is a very potent inhibitor, and is often recommended for patients who have become resistant to other treatments, but also has a relatively harsh side-effect profile.

* The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information

===Mechanism of Action===

When [[HIV]] infects a host, it directs the synthesis of several polyproteins. The maturation of the virus to its infectious form requires that these polyproteins be cleaved to their component proteins by [[HIV Protease]]. The subunits of <scene name='Indinavir/Hiv_p/1'>HIV Protease</scene> come together to form a catalytic tunnel capable of binding the nascent peptides and cleaving them into their mature form. Within this tunnel lies <scene name='Indinavir/Cat/1'>two Asp-Thr-Gly conserved sequences</scene>, which contain the <scene name='Indinavir/Cat/2'>catalytic Asp residues</scene>. These catalytic Asp residues carry out the hydrolytic cleavage of the polyprotein. Indinavir <scene name='Indinavir/Indinavir/2'>binds with great specificity</scene> to these conserved sequences within the HIV Protease tunnel, preventing the nascent polyproteins from entering. Unable to actively cleave the nascent proteins into their appropriate form, HIV is unable to mature and proliferate, allowing the patients immune system to fight off the infection more easily.<ref>PMID:1799632</ref><ref>~~PMID~~:~~15066177~~</ref>

When [[HIV]] infects a host, it directs the synthesis of several polyproteins. The maturation of the virus to its infectious form requires that these polyproteins be cleaved to their component proteins by [[HIV Protease]]. The subunits of <scene name='Indinavir/Hiv_p/1'>HIV Protease</scene> come together to form a catalytic tunnel capable of binding the nascent peptides and cleaving them into their mature form. Within this tunnel lies <scene name='Indinavir/Cat/1'>two Asp-Thr-Gly conserved sequences</scene>, which contain the <scene name='Indinavir/Cat/2'>catalytic Asp residues</scene>. These catalytic Asp residues carry out the hydrolytic cleavage of the polyprotein. Indinavir <scene name='Indinavir/Indinavir/2'>binds with great specificity</scene> to these conserved sequences within the HIV Protease tunnel, preventing the nascent polyproteins from entering. Unable to actively cleave the nascent proteins into their appropriate form, HIV is unable to mature and proliferate, allowing the patients immune system to fight off the infection more easily.<ref>PMID:1799632</ref><ref>doi:10.1038/nrd1907</ref>

===Drug Resistance===

Tipranavir: Difference between revisions

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@@ Line 6: / Line 6: @@
 * Date of FDA Approval (Patent Expiration): 2005 (2015) <br />
 * 2009 Sales: $200 Million
-* Importance: At the time of its approval, it was far more powerful than prior antiretroviral drugs. Has subsequently been largely replaced with newer drugs which are less likely to promote resistance, such as [[Lopinavir]] and [[Atazanavir]]
+* Importance: It was the ninth [[HIV Protease]] inhibitor approved by the FDA for treatment of HIV. It is a very potent inhibitor, and is often recommended for patients who have become resistant to other treatments, but also has a relatively harsh side-effect profile.
 * The following is a list of Pharmacokinetic Parameters. See: [[Pharmaceutical Drugs]] for more information
 ===Mechanism of Action===
-When [[HIV]] infects a host, it directs the synthesis of several polyproteins. The maturation of the virus to its infectious form requires that these polyproteins be cleaved to their component proteins by [[HIV Protease]]. The subunits of <scene name='Indinavir/Hiv_p/1'>HIV Protease</scene> come together to form a catalytic tunnel capable of binding the nascent peptides and cleaving them into their mature form. Within this tunnel lies <scene name='Indinavir/Cat/1'>two Asp-Thr-Gly conserved sequences</scene>, which contain the <scene name='Indinavir/Cat/2'>catalytic Asp residues</scene>. These catalytic Asp residues carry out the hydrolytic cleavage of the polyprotein. Indinavir <scene name='Indinavir/Indinavir/2'>binds with great specificity</scene> to these conserved sequences within the HIV Protease tunnel, preventing the nascent polyproteins from entering. Unable to actively cleave the nascent proteins into their appropriate form, HIV is unable to mature and proliferate, allowing the patients immune system to fight off the infection more easily.<ref>PMID:1799632</ref><ref>PMID:15066177</ref>
+When [[HIV]] infects a host, it directs the synthesis of several polyproteins. The maturation of the virus to its infectious form requires that these polyproteins be cleaved to their component proteins by [[HIV Protease]]. The subunits of <scene name='Indinavir/Hiv_p/1'>HIV Protease</scene> come together to form a catalytic tunnel capable of binding the nascent peptides and cleaving them into their mature form. Within this tunnel lies <scene name='Indinavir/Cat/1'>two Asp-Thr-Gly conserved sequences</scene>, which contain the <scene name='Indinavir/Cat/2'>catalytic Asp residues</scene>. These catalytic Asp residues carry out the hydrolytic cleavage of the polyprotein. Indinavir <scene name='Indinavir/Indinavir/2'>binds with great specificity</scene> to these conserved sequences within the HIV Protease tunnel, preventing the nascent polyproteins from entering. Unable to actively cleave the nascent proteins into their appropriate form, HIV is unable to mature and proliferate, allowing the patients immune system to fight off the infection more easily.<ref>PMID:1799632</ref><ref>doi:10.1038/nrd1907</ref>
 ===Drug Resistance===