6 hours ago, John Cuthber said:

Have you seen the guy to whom RFK Jr plans to put in charge of "researching" autism. David Geier
He worked with his dad, Mark Geier poisoning autistic kids for money.
https://en.wikipedia.org/wiki/Mark_Geier

I wonder why he wants a list of everyone with autism.

Yes they're the worst kind of quacks. The son should be facing criminal charges, and not anywhere children or the levers of my country's healthcare system. This appointment is like putting Ted Bundy in charge of a women's shelter. RFK Jr's brain worm has clearly won.

3 hours ago, Sohan Lalwani said:

Have you read all of the provided papers? I am guessing not. Also your original point is wrong, it does serve as an anti platelet agent. "Trust me bros" don't work

Since you still refuse to engage with your own sources (again), I will help you along the way.

Hirudin is an anti-coagulative product of the salivary glands of the medicinal leech Hirudo medicinalis. It is a powerful and specific thrombin inhibitor. Peptides containing the RGD motif competitively inhibit the binding of fibrinogen to GP IIb/IIIa on the platelets, thus inhibiting platelet aggregation. Results We have constructed a recombinant RGD-hirudin (r-RGD-hirudin) by fusing the tripeptide RGD sequence to the native hirudin (wt-hirudin).

Here the authors say that they have the anti-coaguluation agent hirudin and they wan to add anti-platelet function to it by adding the RGD-motif, which was found to have anti-platelet functions. so kindly explain why the authors felt the need to create a fusion product to add a function, if it was already there to begin with.

I remind you, this is a paper you cited to support your point, and you have not shown that it does and ask others to do the reading for you is just lazy. I will also offer another piece of information: anti-coagulations are generally substances that interfere in the primary clotting cascade. Anti-platelet are substances that primarily interfere with platelet adhesion and interactions. There are overlaps in the blood clot formation, but as you made the distinction between these two, you should be also aware of the differences.

Now kindly go through your references and simply quote the parts that makes you believe that hirudin is acting on these two processes. And again, note that the direct interference into the respective processes is what distinguishes these classes of compounds. I will also note that your second link refers to your first one and the third one is again a synthetic, as I mentioned. I will also add that if you happen to ask AI and force it tell you about the anti-platelet action of hirudin, it will confuse hybrid proteins with native one.

I will suggest that you stop being lazy and either substantiate your points, which could lead to discussions and clarification (and thereby someone could learn something. In fact, I would be curious to see if there was actually a publication showing direct anti-platelet activities (i.e. some direct interactions with thrombocytes), yet afaik all such activities are the result of thrombin inhibition as primary function (and hence the classification as anti-coagulant).

Alternative, if learning or providing is not your goal then perhaps refrain to post half-understood concepts as facts. Such an attitude is a big inhibitor to learning and understanding and rapidly derails discussions, as you can see here.

9 hours ago, John Cuthber said:

Have you seen the guy to whom RFK Jr plans to put in charge of "researching" autism. David Geier
He worked with his dad, Mark Geier poisoning autistic kids for money.
https://en.wikipedia.org/wiki/Mark_Geier

I wonder why he wants a list of everyone with autism.

Also IIRC that guy never even got a license. They are going to pull some random factoids out of their collective arses and then try to create facts by fiat. Public health is looking grim. I have been talking with colleagues and I kind of regret starting to work in this field. It is just getting more depressing by the minute, especially as the stupidity won't remain constrained in the US. In fact, there are already multiple ripples running through global health systems and the one thing we learned from COVID-19 is that we are not ready to deal with such massive challenges very well.

5 minutes ago, CharonY said:

Since you still refuse to engage with your own sources (again), I will help you along the way.

Intriguing, you still didn't answer my statement nor my question.

7 minutes ago, CharonY said:

Since you still refuse to engage with your own sources (again), I will help you along the way.

Here the authors say that they have the anti-coaguluation agent hirudin and they wan to add anti-platelet function to it by adding the RGD-motif, which was found to have anti-platelet functions. so kindly explain why the authors felt the need to create a fusion product to add a function, if it was already there to begin with.

I remind you, this is a paper you cited to support your point, and you have not shown that it does and ask others to do the reading for you is just lazy. I will also offer another piece of information: anti-coagulations are generally substances that interfere in the primary clotting cascade. Anti-platelet are substances that primarily interfere with platelet adhesion and interactions. There are overlaps in the blood clot formation, but as you made the distinction between these two, you should be also aware of the differences.

Now kindly go through your references and simply quote the parts that makes you believe that hirudin is acting on these two processes. And again, note that the direct interference into the respective processes is what distinguishes these classes of compounds. I will also note that your second link refers to your first one and the third one is again a synthetic, as I mentioned. I will also add that if you happen to ask AI and force it tell you about the anti-platelet action of hirudin, it will confuse hybrid proteins with native one.

I will suggest that you stop being lazy and either substantiate your points, which could lead to discussions and clarification (and thereby someone could learn something. In fact, I would be curious to see if there was actually a publication showing direct anti-platelet activities (i.e. some direct interactions with thrombocytes), yet afaik all such activities are the result of thrombin inhibition as primary function (and hence the classification as anti-coagulant).

Alternative, if learning or providing is not your goal then perhaps refrain to post half-understood concepts as facts. Such an attitude is a big inhibitor to learning and understanding and rapidly derails discussions, as you can see here.

Also IIRC that guy never even got a license. They are going to pull some random factoids out of their collective arses and then try to create facts by fiat. Public health is looking grim. I have been talking with colleagues and I kind of regret starting to work in this field. It is just getting more depressing by the minute, especially as the stupidity won't remain constrained in the US. In fact, there are already multiple ripples running through global health systems and the one thing we learned from COVID-19 is that we are not ready to deal with such massive challenges very well.

Leech saliva contains hirudin, an anticoagulant that also indirectly inhibits platelet activation by blocking thrombin. Perhaps this may be better, cite your sources as well

30 minutes ago, CharonY said:

Since you still refuse to engage with your own sources (again), I will help you along the way.

Here the authors say that they have the anti-coaguluation agent hirudin and they wan to add anti-platelet function to it by adding the RGD-motif, which was found to have anti-platelet functions. so kindly explain why the authors felt the need to create a fusion product to add a function, if it was already there to begin with.

I remind you, this is a paper you cited to support your point, and you have not shown that it does and ask others to do the reading for you is just lazy. I will also offer another piece of information: anti-coagulations are generally substances that interfere in the primary clotting cascade. Anti-platelet are substances that primarily interfere with platelet adhesion and interactions. There are overlaps in the blood clot formation, but as you made the distinction between these two, you should be also aware of the differences.

Now kindly go through your references and simply quote the parts that makes you believe that hirudin is acting on these two processes. And again, note that the direct interference into the respective processes is what distinguishes these classes of compounds. I will also note that your second link refers to your first one and the third one is again a synthetic, as I mentioned. I will also add that if you happen to ask AI and force it tell you about the anti-platelet action of hirudin, it will confuse hybrid proteins with native one.

I will suggest that you stop being lazy and either substantiate your points, which could lead to discussions and clarification (and thereby someone could learn something. In fact, I would be curious to see if there was actually a publication showing direct anti-platelet activities (i.e. some direct interactions with thrombocytes), yet afaik all such activities are the result of thrombin inhibition as primary function (and hence the classification as anti-coagulant).

Alternative, if learning or providing is not your goal then perhaps refrain to post half-understood concepts as facts. Such an attitude is a big inhibitor to learning and understanding and rapidly derails discussions, as you can see here.

Also IIRC that guy never even got a license. They are going to pull some random factoids out of their collective arses and then try to create facts by fiat. Public health is looking grim. I have been talking with colleagues and I kind of regret starting to work in this field. It is just getting more depressing by the minute, especially as the stupidity won't remain constrained in the US. In fact, there are already multiple ripples running through global health systems and the one thing we learned from COVID-19 is that we are not ready to deal with such massive challenges very well.

“Yet afaik all such activities are the result of thrombin inhibition as primary function (and hence the classification as anti-coagulant).”

At first glance, this seems reasonable: hirudin is classified as an anti-coagulant, and its mechanism is thrombin inhibition. However, your factual inaccuracy lies in the implied claim that any anti-platelet activity is only a secondary, indirect result of coagulation inhibition, and that hirudin has no direct influence on platelet-related processes. That’s not entirely correct.

Thrombin is not only a central player in the coagulation cascade; it also acts as one of the most potent activators of platelets. It activates platelets by binding to protease-activated receptors (PAR-1 and PAR-4) on the platelet surface. This is a direct receptor-ligand interaction, not a downstream consequence of fibrin generation.

So when hirudin binds to thrombin and neutralizes it, it is directly preventing thrombin from binding to those receptors and activating platelets. In other words, hirudin is interfering with a specific and direct pathway of platelet activation.

Therefore, hirudin is not just "indirectly" affecting platelets by suppressing fibrin formation, it is mechanistically blocking thrombin-mediated platelet activation at the receptor level. This is still considered an anti-platelet effect, even if the drug is not classed as an anti-platelet agent per se.

I DO CONCEDE, I COULD HAVE BEEN MORE NUANCED

Please counterclaim or correct if possible, also please stop with the “if you ask AI” or “I could tell you’re using ai” because 1, there is no way to verify I used it, and 2, it’s just irrelevant and annoying.

With all due respect since you seem like a fairly pleasant user and I think you would understand, it’s pissing me off with the ai stuff.

24 minutes ago, Sohan Lalwani said:

Intriguing, you still didn't answer my statement nor my question.

What statement? Whether I read the papers? I mentioned what is in there and how it does not show your claim. I will again note that despite them being your sources you have not actually showed how it supports or your argument.

26 minutes ago, Sohan Lalwani said:

Perhaps this may be better, cite your sources as well

I remind you that you made the claim. I have mentioned that hirudin works on thrombin and acts on an element of the anti-coagulation cascade and is therefore classified as an anti-coagulant. I cannot show you papers that it does not interact with thrombocytes, because well, they don't.

I mentioned before that all anti-platelet activities I am aware of are because of thrombin interactions. And this is because of thrombin is also an platelet activator via PARs, which then activate the process. As you now acknowledged any anti-platelet activity are indirect and hence, they are generally not categorized an anti-platelet agent as you claimed originally. And again, if you had read your first paper, you should have asked yourself why did the add an anti-platelet moiety to a molecule that supposedly has already such activities? You may also want to read a chapter on antiplatelets: https://www.ncbi.nlm.nih.gov/books/NBK537062/

Then look at the passage about glycoprotein inhibitors, which work on GPIIb-IIIa receptors. Then actually open up your first link (or at least the abstract) and see if you notice something.

I will note that the classification of anti-coagulant and antiplatelet drugs is a bit less straightforward as they were not based on a full understanding of the molecular mechanisms and targets.

🛌

2 minutes ago, CharonY said:

What statement? Whether I read the papers? I mentioned what is in there and how it does not show your claim. I will again note that despite them being your sources you have not actually showed how it supports or your argument.

I remind you that you made the claim. I have mentioned that hirudin works on thrombin and acts on an element of the anti-coagulation cascade and is therefore classified as an anti-coagulant. I cannot show you papers that it does not interact with thrombocytes, because well, they don't.

I mentioned before that all anti-platelet activities I am aware of are because of thrombin interactions. And this is because of thrombin is also an platelet activator via PARs, which then activate the process. As you now acknowledged any anti-platelet activity are indirect and hence, they are generally not categorized an anti-platelet agent as you claimed originally. And again, if you had read your first paper, you should have asked yourself why did the add an anti-platelet moiety to a molecule that supposedly has already such activities? You may also want to read a chapter on antiplatelets: https://www.ncbi.nlm.nih.gov/books/NBK537062/

Then look at the passage about glycoprotein inhibitors, which work on GPIIb-IIIa receptors. Then actually open up your first link (or at least the abstract) and see if you notice something.

I will note that the classification of anti-coagulant and antiplatelet drugs is a bit less straightforward as they were not based on a full understanding of the molecular mechanisms and targets.

I am off to bed so here’s a sort of recap regarding my points

I appreciate the thoughtful distinction you've drawn between anti-coagulant and anti-platelet mechanisms—this is indeed a critical conceptual divide in hemostasis research. However, there is a factual inaccuracy in your assertion that “all such activities [of hirudin] are the result of thrombin inhibition as primary function,” with the implication that any observed anti-platelet effects are necessarily indirect or secondary to its anti-coagulant role. This mischaracterizes the specific mechanistic role thrombin plays in platelet activation and, consequently, how hirudin modulates that process.

Thrombin is not merely a terminal effector of fibrin formation; it is also one of the most potent physiological activators of platelets. It exerts this effect through direct interaction with protease-activated receptors (PAR-1 and PAR-4) on the platelet surface, initiating intracellular signaling cascades that result in platelet shape change, degranulation, and integrin activation—central steps in thrombus formation. This is not a downstream effect of clot formation, but a primary, receptor-mediated cellular activation process.

Hirudin, as a highly specific direct thrombin inhibitor, binds both the active site and exosite I of thrombin with high affinity. By neutralizing thrombin’s proteolytic activity, hirudin directly prevents thrombin from engaging its platelet receptors. Therefore, hirudin’s interference with thrombin-mediated platelet activation is not merely a side effect of reduced fibrin formation; it is a primary, mechanistically direct interruption of a major platelet activation pathway. Multiple experimental studies support this: platelet aggregation assays in vitro consistently show that hirudin prevents thrombin-induced aggregation, even in the absence of fibrinogen or other coagulation factors.

Thus, while hirudin is accurately classified as an anti-coagulant, its effect on platelets—specifically those mediated through thrombin-PAR interactions—represents a direct and biologically significant anti-platelet mechanism. The development of fusion constructs with RGD motifs is not meant to introduce the first anti-platelet effect to hirudin, but rather to expand its scope by targeting additional pathways, such as integrin-mediated adhesion, which hirudin does not affect on its own.

In short, your assertion overlooks the well-documented fact that thrombin is itself a direct platelet agonist, and therefore, any compound that specifically neutralizes thrombin—such as hirudin—does in fact exert direct anti-platelet effects through a well-defined molecular mechanism. While your caution against conflating engineered fusion proteins with native bioactivity is absolutely justified and appreciated, the underlying biology of thrombin and its dual role in coagulation and platelet activation necessitates a more nuanced interpretation of hirudin’s pharmacodynamics.

I hope this clarification adds constructively to the discussion.

Good night @CharonY 🛌

2 minutes ago, CharonY said:

What statement? Whether I read the papers? I mentioned what is in there and how it does not show your claim. I will again note that despite them being your sources you have not actually showed how it supports or your argument.

I remind you that you made the claim. I have mentioned that hirudin works on thrombin and acts on an element of the anti-coagulation cascade and is therefore classified as an anti-coagulant. I cannot show you papers that it does not interact with thrombocytes, because well, they don't.

I mentioned before that all anti-platelet activities I am aware of are because of thrombin interactions. And this is because of thrombin is also an platelet activator via PARs, which then activate the process. As you now acknowledged any anti-platelet activity are indirect and hence, they are generally not categorized an anti-platelet agent as you claimed originally. And again, if you had read your first paper, you should have asked yourself why did the add an anti-platelet moiety to a molecule that supposedly has already such activities? You may also want to read a chapter on antiplatelets: https://www.ncbi.nlm.nih.gov/books/NBK537062/

Then look at the passage about glycoprotein inhibitors, which work on GPIIb-IIIa receptors. Then actually open up your first link (or at least the abstract) and see if you notice something.

I will note that the classification of anti-coagulant and antiplatelet drugs is a bit less straightforward as they were not based on a full understanding of the molecular mechanisms and targets.

I was wrong about the classification, they are not primarily classified in such a way.

50 minutes ago, Sohan Lalwani said:

not a downstream consequence of fibrin generation.

No one mentioned fibrin generation. The secondary comes from the action of hirudin on thrombin then hirudin interaction via PARs and then platelet activation.

52 minutes ago, Sohan Lalwani said:

Please counterclaim or correct if possible, also please stop with the “if you ask AI” or “I could tell you’re using ai” because 1, there is no way to verify I used it, and 2, it’s just irrelevant and annoying.

This is mostly a push for you to stop just making a claim an throw up links that in no way support your claim. Again, your source contradicts your logic and yet you keep sidestepping that. There is no way to figure out why you make those claims and/or use these resources, which is just incredibly lazy and it really doesn't matter if it was AI or not. You are effectively making the same mistakes as a the AI summary from google is making.

2 minutes ago, Sohan Lalwani said:

I appreciate the thoughtful distinction you've drawn between anti-coagulant and anti-platelet mechanisms—this is indeed a critical conceptual divide in hemostasis research. However, there is a factual inaccuracy in your assertion that “all such activities [of hirudin] are the result of thrombin inhibition as primary function,” with the implication that any observed anti-platelet effects are necessarily indirect or secondary to its anti-coagulant role. This mischaracterizes the specific mechanistic role thrombin plays in platelet activation and, consequently, how hirudin modulates that process.

Thrombin is not merely a terminal effector of fibrin formation; it is also one of the most potent physiological activators of platelets. It exerts this effect through direct interaction with protease-activated receptors (PAR-1 and PAR-4) on the platelet surface, initiating intracellular signaling cascades that result in platelet shape change, degranulation, and integrin activation—central steps in thrombus formation. This is not a downstream effect of clot formation, but a primary, receptor-mediated cellular activation process.

Hirudin, as a highly specific direct thrombin inhibitor, binds both the active site and exosite I of thrombin with high affinity. By neutralizing thrombin’s proteolytic activity, hirudin directly prevents thrombin from engaging its platelet receptors. Therefore, hirudin’s interference with thrombin-mediated platelet activation is not merely a side effect of reduced fibrin formation; it is a primary, mechanistically direct interruption of a major platelet activation pathway. Multiple experimental studies support this: platelet aggregation assays in vitro consistently show that hirudin prevents thrombin-induced aggregation, even in the absence of fibrinogen or other coagulation factors.

Thus, while hirudin is accurately classified as an anti-coagulant, its effect on platelets—specifically those mediated through thrombin-PAR interactions—represents a direct and biologically significant anti-platelet mechanism. The development of fusion constructs with RGD motifs is not meant to introduce the first anti-platelet effect to hirudin, but rather to expand its scope by targeting additional pathways, such as integrin-mediated adhesion, which hirudin does not affect on its own.

In short, your assertion overlooks the well-documented fact that thrombin is itself a direct platelet agonist, and therefore, any compound that specifically neutralizes thrombin—such as hirudin—does in fact exert direct anti-platelet effects through a well-defined molecular mechanism. While your caution against conflating engineered fusion proteins with native bioactivity is absolutely justified and appreciated, the underlying biology of thrombin and its dual role in coagulation and platelet activation necessitates a more nuanced interpretation of hirudin’s pharmacodynamics.

I hope this clarification adds constructively to the discussion.

And if that is a summary of your thoughts why would you add explanation to it that are neither claimed in this thread nor are the relevant to the aspect under discussion. This whole text just shows that there is no understanding and no desire to understand the key issues (as minor as they are). The way it is written just throws together factoids and related elements, even if many of them are simply irrelevant (just as the mentioning fibrin, though we never discussed it, just happens to be the activity in the coagulation cascade but is not relevant to the discussion of potential anti-platelet function which happens via thrombin. And whoever wrote the text clearly lacks any awareness as they continue happily to discuss just that.

As such it is clear that there is no meaningful discussion to be had and I might just yell at google.

9 hours ago, CharonY said:

No one mentioned fibrin generation. The secondary comes from the action of hirudin on thrombin then hirudin interaction via PARs and then platelet activation.

That reference was an attempt to preempt a common misunderstanding in discussions about anti-coagulants vs anti-platelets—not to misrepresent your position. I’ll own that the inclusion was unnecessary in this context and I appreciate you pointing it out.

9 hours ago, CharonY said:

No one mentioned fibrin generation. The secondary comes from the action of hirudin on thrombin then hirudin interaction via PARs and then platelet activation.

This is mostly a push for you to stop just making a claim an throw up links that in no way support your claim. Again, your source contradicts your logic and yet you keep sidestepping that. There is no way to figure out why you make those claims and/or use these resources, which is just incredibly lazy and it really doesn't matter if it was AI or not. You are effectively making the same mistakes as a the AI summary from google is making.

And if that is a summary of your thoughts why would you add explanation to it that are neither claimed in this thread nor are the relevant to the aspect under discussion. This whole text just shows that there is no understanding and no desire to understand the key issues (as minor as they are). The way it is written just throws together factoids and related elements, even if many of them are simply irrelevant (just as the mentioning fibrin, though we never discussed it, just happens to be the activity in the coagulation cascade but is not relevant to the discussion of potential anti-platelet function which happens via thrombin. And whoever wrote the text clearly lacks any awareness as they continue happily to discuss just that.

As such it is clear that there is no meaningful discussion to be had and I might just yell at google.

However, the central point I was addressing still stands: the mechanism by which hirudin inhibits platelet activation is not simply a downstream effect of it being an anti-coagulant. The confusion seems to lie in labeling thrombin-PAR signaling as an "indirect" or “secondary” target of hirudin, when in fact it is a primary physiological function of thrombin. Thrombin binding to PAR-1 and PAR-4 on platelets is not contingent on thrombin’s role in the broader coagulation cascade, nor does it depend on fibrin generation. It is a direct receptor-ligand interaction, and it's this interaction that hirudin blocks.

So the nuance is this: inhibiting thrombin is not “indirect” just because the effect on platelets happens through thrombin. If thrombin is a direct agonist of platelets, and hirudin directly inhibits thrombin, then hirudin is directly blocking a platelet activation pathway. That’s not the same as calling hirudin an anti-platelet drug in the pharmacological sense (like aspirin), but it is factually incorrect to dismiss its effect on platelets as merely indirect or secondary.

Ultimately, I’m not here to "win" a disagreement—I’m genuinely trying to understand this with scientific clarity. If there are studies you feel contradict that interpretation, I’d be glad to read and discuss them. Otherwise, I still believe the distinction I’ve outlined reflects the current understanding of thrombin biology and hirudin pharmacodynamics.

Thanks again for engaging—this is how science moves forward, even in disagreement

9 hours ago, CharonY said:

This is mostly a push for you to stop just making a claim an throw up links that in no way support your claim. Again, your source contradicts your logic and yet you keep sidestepping that. There is no way to figure out why you make those claims and/or use these resources, which is just incredibly lazy and it really doesn't matter if it was AI or not. You are effectively making the same mistakes as a the AI summary from google is making.

I’m not even going to engage with this anymore, all I can say is that it’s annoying as shit

On 5/14/2025 at 7:26 PM, Sohan Lalwani said:

I am very confused regarding a certain situation. RFK Jr. supports that children should be healthy, he also has a very strong anti vaccine stance. HOW DOES THAT MAKE SENSE

It doesn't, but Trump has made other appointments that have also left others confused.

1 hour ago, paulsutton said:

It doesn't, but Trump has made other appointments that have also left others confused.

😵‍💫

On 5/17/2025 at 6:35 AM, Sohan Lalwani said:

🛌

I am off to bed so here’s a sort of recap regarding my points

I appreciate the thoughtful distinction you've drawn between anti-coagulant and anti-platelet mechanisms—this is indeed a critical conceptual divide in hemostasis research. However, there is a factual inaccuracy in your assertion that “all such activities [of hirudin] are the result of thrombin inhibition as primary function,” with the implication that any observed anti-platelet effects are necessarily indirect or secondary to its anti-coagulant role. This mischaracterizes the specific mechanistic role thrombin plays in platelet activation and, consequently, how hirudin modulates that process.

Thrombin is not merely a terminal effector of fibrin formation; it is also one of the most potent physiological activators of platelets. It exerts this effect through direct interaction with protease-activated receptors (PAR-1 and PAR-4) on the platelet surface, initiating intracellular signaling cascades that result in platelet shape change, degranulation, and integrin activation—central steps in thrombus formation. This is not a downstream effect of clot formation, but a primary, receptor-mediated cellular activation process.

Hirudin, as a highly specific direct thrombin inhibitor, binds both the active site and exosite I of thrombin with high affinity. By neutralizing thrombin’s proteolytic activity, hirudin directly prevents thrombin from engaging its platelet receptors. Therefore, hirudin’s interference with thrombin-mediated platelet activation is not merely a side effect of reduced fibrin formation; it is a primary, mechanistically direct interruption of a major platelet activation pathway. Multiple experimental studies support this: platelet aggregation assays in vitro consistently show that hirudin prevents thrombin-induced aggregation, even in the absence of fibrinogen or other coagulation factors.

Thus, while hirudin is accurately classified as an anti-coagulant, its effect on platelets—specifically those mediated through thrombin-PAR interactions—represents a direct and biologically significant anti-platelet mechanism. The development of fusion constructs with RGD motifs is not meant to introduce the first anti-platelet effect to hirudin, but rather to expand its scope by targeting additional pathways, such as integrin-mediated adhesion, which hirudin does not affect on its own.

In short, your assertion overlooks the well-documented fact that thrombin is itself a direct platelet agonist, and therefore, any compound that specifically neutralizes thrombin—such as hirudin—does in fact exert direct anti-platelet effects through a well-defined molecular mechanism. While your caution against conflating engineered fusion proteins with native bioactivity is absolutely justified and appreciated, the underlying biology of thrombin and its dual role in coagulation and platelet activation necessitates a more nuanced interpretation of hirudin’s pharmacodynamics.

I hope this clarification adds constructively to the discussion.

Good night @CharonY 🛌

I was wrong about the classification, they are not primarily classified in such a way.

You didn't write that. The style - and the obsequious opening - are quite at odds with your own. You are quoting some other source, without attribution. You have done this before, introducing egregious errors in the process. If you quote other sources you should reference them.

Edited May 19May 19 by exchemist

6 hours ago, exchemist said:

You didn't write that. The style - and the obsequious opening - are quite at odds with your own. You are quoting some other source, without attribution. You have done this before, introducing egregious errors in the process. If you quote other sources you should reference them.

Until what your saying is objectively provable, it’s better to not say anything at all

Classic non-denial denial

1 hour ago, iNow said:

Classic non-denial denial

what astronomically helpful input this is

5 hours ago, iNow said:

Classic non-denial denial

Quite so.

3 hours ago, exchemist said:

Quite so.

Sure sure buddy