What's new

85% of the World's HIV/AIDS Antiretroviral Drugs Made in India

.
And we are also earning a neat 15 billion dollars per year in exports

NOT bad at all

Indian companies, both pharma and biotech, have made a name for themselves across most of the developing world and increasingly middle income countries for high quality low cost medicines.

Obviously this is not going to be increasingly liked by "the system."

Because "the system" has been evergreening patents and milking a dry tit for decades now, as the blckbuster pipeline has all but dried up, and the MABs present the largest grossers today. And that too is on its way out post 2017 forward.
 
.
Indian companies, both pharma and biotech, have made a name for themselves across most of the developing world and increasingly middle income countries for high quality low cost medicines.

Obviously this is not going to be increasingly liked by "the system."

Because "the system" has been evergreening patents and milking a dry tit for decades now, as the blckbuster pipeline has all but dried up, and the MABs present the largest grossers today. And that too is on its way out post 2017 forward.

During that GLEEVEC case ; That time there was a lot of debate

I read that most of the so called new medicines are just a little re jig
or slight change of ingredients and components

Hence dont qualify to be called as new medicines

By the way what is an MAB ; that you referred to
 
.
During that GLEEVEC case ; That time there was a lot of debate

I read that most of the so called new medicines are just a little re jig
or slight change of ingredients and components

Hence dont qualify to be called as new medicines

By the way what is an MAB ; that you referred to

That's exactly what is understood in the industry as evergreening.

Monclonal Antibody.
 
. .
Which part of his post does he claim to be a doctor or pharmacist?

He mentioned "If i have 100 patients" i.e hypothetical scenario

Just because a Pakistani doesn't approve of your views, you suspect his nationality?

Seems like paranoia is getting the best of you or you have little confidence in your own countrymen
he posed as 'medicen' importers who want to make money. It does not even mean he is an importer, let alone doctor.
 
. . .
he posed as 'medicen' importers who want to make money. It does not even mean he is an importer, let alone doctor.
a student or businessman(I presume) unable to correctly construct a sentence!

Since when students/businessmen living in UK started to write such english?

@WebMister Can you please check this member's IP address?
 
.
a student or businessman(I presume) unable to correctly construct a sentence!

Since when students/businessmen living in UK started to write such english?

@WebMister Can you please check this member's IP address?
tu sahi doctor hai.. poor handwriting :p:
 
. .
@Syed.Ali.Haider @doppelganger

Here is a New York times article regarding the Gleevec case

This article is SUPPORTIVE of India's case

http://www.nytimes.com/2013/04/05/o...dia-clarifies-law-in-novartis-decision.html?_

This line from the story is important:

capture_001_18072015_094526.jpg
 
.
How medicine attacks a virus? in layman's language...

I will talk how it works against HIV, for this is my area of expertise.

Target 1. In order to infect cells, HIV has to interact with the cells first. Only certain types of cells can be infected by HIV and it is because these cells contain protein molecules on their surface that are recognized by HIV. These molecules are called ‘receptors’. HIV also has certain proteins on its surface that interact with the ‘receptors’ on the cells it is going to infect. If HIV can be stopped from interacting with host cells, infection will not take place. In this particular scenario, we can either mask HIV molecules (gp120 and gp41) or molecules (CD4, CCR5, CXCR4) on the surface of host cells. Drugs called ‘Entry inhibitors’ (or fusion inhibitors) target these steps.

Target 2. Once an HIV manages to interact with the host cell via receptors, it will get itself attached with the host cell and inject a body called ‘capsid’ that contains HIV genome and various helping proteins. Once the ‘capsid’ is inside the cell, it disassembles in a coordinated fashion to release viral genome, which later gets integrated into host cell DNA. If we could stop the ‘capsid’ from disassembling or accelerate its assembly, the viral genome will not be released and not get integrated into the host DNA. Thus drugs can be designed to target these steps. At present no FDA approved drugs available to target capsid.

Target 3. Once the capsid is disassembled in a coordinated fashion, the viral genome that is in the form of a single stranded RNA is released into cytoplasm. This RNA is made into a double stranded DNA by the help of a viral enzyme called reverse transcriptase (RT). This step is crucial because viral genome can only get integrated into host DNA if it is in the form of a double stranded DNA. Thus drugs can be designed to target viral RT so that RNA genome does not get made into DNA. Drugs called ‘reverse transcriptase inhibitors’ target these steps.

Target 4. Once the RNA genome is converted into DNA, it gets inserted into host genome by the help of a viral enzyme called integrase (IN). If we could target this enzyme, we can stop the integration of viral DNA into the host genome and therefore new viruses will not be made. Drugs called ‘Integrase inhibitors’ target these steps.

Target 5. Once the viral DNA gets integrated into host DNA, it starts making viral proteins. These proteins are generally made as poly proteins i.e. a large protein that can be broken down into smaller functional proteins. There are three such poly proteins called Gag, Pol, and Env. In order to break them into smaller functional proteins, a viral enzyme called ‘protease’ is made by viral genome. If HIV protease could be stopped from breaking down poly proteins, the new viral particles will not be assembled. Hence drugs called ‘Protease inhibitors’ are designed to target these steps.

So as you see, HIV can be attacked at several steps of its lifecycle. HART (highly active retroviral therapy) regimen is therefore composed of at-least three drugs targeting different steps of HIV life cycle as described above.

@anant_s @Slav Defence
 
.
How medicine attacks a virus? in layman's language...

I will talk how it works against HIV, for this is my area of expertise.

Target 1. In order to infect cells, HIV has to interact with the cells first. Only certain types of cells can be infected by HIV and it is because these cells contain protein molecules on their surface that are recognized by HIV. These molecules are called ‘receptors’. HIV also has certain proteins on its surface that interact with the ‘receptors’ on the cells it is going to infect. If HIV can be stopped from interacting with host cells, infection will not take place. In this particular scenario, we can either mask HIV molecules (gp120 and gp41) or molecules (CD4, CCR5, CXCR4) on the surface of host cells. Drugs called ‘Entry inhibitors’ (or fusion inhibitors) target these steps.

Target 2. Once an HIV manages to interact with the host cell via receptors, it will get itself attached with the host cell and inject a body called ‘capsid’ that contains HIV genome and various helping proteins. Once the ‘capsid’ is inside the cell, it disassembles in a coordinated fashion to release viral genome, which later gets integrated into host cell DNA. If we could stop the ‘capsid’ from disassembling or accelerate its assembly, the viral genome will not be released and not get integrated into the host DNA. Thus drugs can be designed to target these steps. At present no FDA approved drugs available to target capsid.

Target 3. Once the capsid is disassembled in a coordinated fashion, the viral genome that is in the form of a single stranded RNA is released into cytoplasm. This RNA is made into a double stranded DNA by the help of a viral enzyme called reverse transcriptase (RT). This step is crucial because viral genome can only get integrated into host DNA if it is in the form of a double stranded DNA. Thus drugs can be designed to target viral RT so that RNA genome does not get made into DNA. Drugs called ‘reverse transcriptase inhibitors’ target these steps.

Target 4. Once the RNA genome is converted into DNA, it gets inserted into host genome by the help of a viral enzyme called integrase (IN). If we could target this enzyme, we can stop the integration of viral DNA into the host genome and therefore new viruses will not be made. Drugs called ‘Integrase inhibitors’ target these steps.

Target 5. Once the viral DNA gets integrated into host DNA, it starts making viral proteins. These proteins are generally made as poly proteins i.e. a large protein that can be broken down into smaller functional proteins. There are three such poly proteins called Gag, Pol, and Env. In order to break them into smaller functional proteins, a viral enzyme called ‘protease’ is made by viral genome. If HIV protease could be stopped from breaking down poly proteins, the new viral particles will not be assembled. Hence drugs called ‘Protease inhibitors’ are designed to target these steps.

So as you see, HIV can be attacked at several steps of its lifecycle. HART (highly active retroviral therapy) regimen is therefore composed of at-least three drugs targeting different steps of HIV life cycle as described above.

@anant_s @Slav Defence
Our country has been plaqued by this scourge. ARVs have done a huge turnaround to people's lives. In addition lifestyle changes are mandatory
 
.
How medicine attacks a virus? in layman's language...

I will talk how it works against HIV, for this is my area of expertise.

Target 1. In order to infect cells, HIV has to interact with the cells first. Only certain types of cells can be infected by HIV and it is because these cells contain protein molecules on their surface that are recognized by HIV. These molecules are called ‘receptors’. HIV also has certain proteins on its surface that interact with the ‘receptors’ on the cells it is going to infect. If HIV can be stopped from interacting with host cells, infection will not take place. In this particular scenario, we can either mask HIV molecules (gp120 and gp41) or molecules (CD4, CCR5, CXCR4) on the surface of host cells. Drugs called ‘Entry inhibitors’ (or fusion inhibitors) target these steps.

Target 2. Once an HIV manages to interact with the host cell via receptors, it will get itself attached with the host cell and inject a body called ‘capsid’ that contains HIV genome and various helping proteins. Once the ‘capsid’ is inside the cell, it disassembles in a coordinated fashion to release viral genome, which later gets integrated into host cell DNA. If we could stop the ‘capsid’ from disassembling or accelerate its assembly, the viral genome will not be released and not get integrated into the host DNA. Thus drugs can be designed to target these steps. At present no FDA approved drugs available to target capsid.

Target 3. Once the capsid is disassembled in a coordinated fashion, the viral genome that is in the form of a single stranded RNA is released into cytoplasm. This RNA is made into a double stranded DNA by the help of a viral enzyme called reverse transcriptase (RT). This step is crucial because viral genome can only get integrated into host DNA if it is in the form of a double stranded DNA. Thus drugs can be designed to target viral RT so that RNA genome does not get made into DNA. Drugs called ‘reverse transcriptase inhibitors’ target these steps.

Target 4. Once the RNA genome is converted into DNA, it gets inserted into host genome by the help of a viral enzyme called integrase (IN). If we could target this enzyme, we can stop the integration of viral DNA into the host genome and therefore new viruses will not be made. Drugs called ‘Integrase inhibitors’ target these steps.

Target 5. Once the viral DNA gets integrated into host DNA, it starts making viral proteins. These proteins are generally made as poly proteins i.e. a large protein that can be broken down into smaller functional proteins. There are three such poly proteins called Gag, Pol, and Env. In order to break them into smaller functional proteins, a viral enzyme called ‘protease’ is made by viral genome. If HIV protease could be stopped from breaking down poly proteins, the new viral particles will not be assembled. Hence drugs called ‘Protease inhibitors’ are designed to target these steps.

So as you see, HIV can be attacked at several steps of its lifecycle. HART (highly active retroviral therapy) regimen is therefore composed of at-least three drugs targeting different steps of HIV life cycle as described above.

@anant_s @Slav Defence

Sir,excellent post.
However,I have a question in my mind.What if we prepare vaccines by using viruses which simply alters cell's genetic code in such a way so that it becomes non permissive ie changing up receptor sites which cannot be recognized by viral protein?

Regards
 
Last edited:
.

Latest posts

Country Latest Posts

Back
Top Bottom