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The fight against cancer is important. And, scientists know it. This is why they haven’t stopped searching for new ways to fight this condition, stopping the uncontrolled cell growth, and helping people come out as the winners. Research is constantly being done, and new methods are being developed, meaning that chemotherapy is not the only course of treatment nowadays, although it is still, without a doubt, an important one.

Having been thinking about how to actually target cancer cells more specifically, while keeping the healthy tissue unharmed, and pretty much unaffected, scientists have begun developing targeted therapies. And, what those usually do is they target the molecular switches that are responsible for pretty much sending the growth and division signals to cancer cells, thus making them spread. This has opened up the doors to plenty of new research options, and plenty of new drug development options.

And, among others, the IGF-1R protein is one of the main targets in those, well, targeted therapies. It is a protein that can be found on the surface of many cells. And, when it is activated, it sends signals to cells that it is time to grow, divide, as well as avoid death. This can cause a lot of problems when we are talking about cancer cells, because the main idea behind treatment options is to stop the growth and division of those cells, and to kill them, which is what this protein can make difficult.

This is why one targeted approach consists of, well, targeting the IGF-1R protein specifically. And, well, Linsitinib (OSI-906) IGF-1R inhibitor, an experimental drug, has been designed with that purpose specifically. The hope behind this drug is that it will slow down and kill those cancer cells that heavily depend on this particular protein signaling. This kind of a drug would, therefore, definitely help in cancer treatment, leading to better patient outcomes, as well as fewer side effects.

Since you are here, it is probably safe to say that you’ve heard of this experimental drug already, and that you’re now interested in learning a bit more about it. Perhaps you’re a researcher yourself, and you want to get a clearer picture on how it all works, or potentially even include this drug in your current or future studies. Whatever the case, you have some questions on your mind, and we are now going to try and answer them for you, hoping to shed more light on Linsitinib (OSI-906) IGF-1R inhibitor, leading you towards understanding it better.

What Is Linsitinib (OSI-906) IGF-1R inhibitor?

It is probably not a surprise that we are going to begin with this basic question. That is, the question of what Linsitinib (OSI-906) IGF-1R inhibitor actually is. After all, there would be no point in digging into details if you’re not familiar with the basics. So, let us cut to the chase and make things clear right away.

To put it simply, Linsitinib (OSI-906) IGF-1R inhibitor is a small molecule inhibitor that is studied for cancer treatments. It is made in the form of a pill, meaning that it is taken orally, which is much more convenient for patients than injections or infusions. While it is still not approved for standard therapy, and it is, therefore, intended for research and experimental use only, research shows that it could have great potential, and that it could, in the future, open up the doors towards a different approach to cancer treatment. If you’re a researcher, you want to find Linsitinib (OSI-906) IGF-1R inhibitor with a very high purity level, so make sure that you’re choosing the right supplier when buying it.

How Does It Work?

Onto the next important question. How does Linsitinib (OSI-906) IGF-1R inhibitor actually work? Basically, it binds to the intracellular kinase domain of IGF-1R, thus preventing the receptor from activating itself after ligand binding. Since this receptor cannot be activated, it cannot send the signals it usually sends to certain pathways downstream, pathways that tell the cells to survive, divide and grow.

As it should be clear already, stopping this signaling can result in stopping the cancer cells from, well, dividing, growing, and even surviving. And, when the cells are deprived of those signals, they can not only get stuck in a non-dividing state, but also undergo apoptosis, which is basically a form of cell death. So, it is clear how this drug can have a great potential in cancer treatment.

Apart from that, another thing may also be worth mentioning. Basically, Linsitinib (OSI-906) IGF-1R inhibitor can also partially inhibit the insulin receptor (IR). And, this can affect the balance of growth and metabolic signaling in cells, which is also rather important. Click this to learn some more about it in general. 

Why Is Targeting IGF-1R So Important?

Now, if you’re wondering why targeting IGF-1R is so important in the first place, let us answer that question as well. Basically, we are talking about a cell surface receptor that has an important role in normal cells, sending those growth, survival and reproduction signals. But, those are the signals that you don’t want in cancer cells, and the truth is that many tumors display the overexpression of this receptor, meaning that it is too active, which results in continuous growth signaling. Targeting it can stop this kind of uncontrolled signaling, and thus prevent tumor growth and metastasis.

What Are the Potential Advantages of This Drug?

Finally, let us quickly understand the potential advantages of this drug. I am saying potential because we’re talking about a drug that is still in the experimental stages. So, for one thing, Linsitinib (OSI-906) IGF-1R inhibitor aims at specific pathways, rather than everything at once, which makes it a great targeted therapy tool.

Then, it is taken orally, which is undoubtedly an important benefit as well. And, of course, another great thing is that it can be used in combination with other therapies, in order to enhance effectiveness and overcome resistance. On top of it all, some research shows that it may be applicable outside oncology as well, but that still has to be studied more thoroughly.