Chemotherapy and radiation were, in the past, the only available options in the fight against cancer. Things are, however, changing in this area over the last few decades, and scientists are nowadays designing smart drugs that actually target specific molecules in our bodies. Of course, those molecules that are responsible for helping cancer cells grow and divide. Learn more about the division of cells in the human body in general, as that could also help you understand what happens with cancer cells as well.
Now, as you may have guessed it already, there are numerous different molecules that cancer cells can depend on, meaning that scientists cannot simply research one of them and be done with it. This is why you may have come across various types of studies and research processes, aiming at understanding various molecules and signaling pathways in the body. After all, scientists are trying to understand most of those processes, as that is sure to help them get a clearer picture of what actually happens with those cancer cells inside our bodies, what they depend on, as well as how to treat them.
And, without a doubt, one of the most important discoveries here was the fact that those cancer cells depend on angiogenesis, which is basically the process of forming new blood vessels. They depend on this process for survival, as without it, they cannot get enough oxygen or other nutrients that they need in order to keep growing. Well, uncovering the fact that angiogenesis plays an important role in tumor survival has opened up new doors for further research.
To cut right to the chase, scientists have understood this type of dependence of cancer cells on angiogenesis, which made them interested in studying that process more. And, more specifically, it made them interested in developing certain drugs that could potentially affect the angiogenesis process, preventing it from doing its work, and thus promoting tumor cell death, instead of survival. It is definitely no wonder that angiogenesis has become an interesting and a crucial target in those cancer related researches.
Well, scientists did undeniably manage to develop certain drugs that could target this particular process. And, Semaxanib (SU5416) VEGFR2 inhibitor was, without a doubt, one of them. If you have come across it today, then chances are that you want to learn a bit more about it and understand what it is and how it works, as well as what kind of a role it has played in cancer treatment in general. Perhaps you are a researcher, or a future researcher, yourself, or simply a person who likes to learn about these things, and whatever the case is there, the fact that you’re here tells me that you undeniably want to understand Semaxanib (SU5416) VEGFR2 inhibitor better, so let us now talk about it in more details.
What Is Semaxanib (SU5416) VEGFR2 Inhibitor?
Unsurprisingly, the first thing we have to do is make sure that you actually understand what Semaxanib (SU5416) VEGFR2 inhibitor is. After all, there is absolutely no point in talking about how it works and why it is important at all, if you don’t even understand what it is in the first place. And, well, this shouldn’t be difficult to understand. So, let us cut right to the chase and tell you what you need to know.
Basically, Semaxanib (SU5416) VEGFR2 inhibitor is a small molecule drug that has been developed in the 1990s, in an effort to block enzymes known as tyrosine kinases. Those specific enzymes are pretty much like the “on” and “off” switches in the cells, sending them signals that can control their movement, growth and survival. And, when these particular switches get basically stuck on the “on” position, which is something that happens in cancer, those cells grow uncontrollably, putting the person in danger, and making it difficult to fight this condition.
Now, among others, VEGFR2 is one of the most important tyrosine kinases that is responsible for blood vessel growth. To put it simply, it is located on the surface of those cells that make up blood vessels. And, when it gets switched on, through a natural signal called VEGF binding to it, it pretty much tells the cells to grow and to make new vessels.
This kind of introductory talk about tyrosine kinases and VEGFR2 specifically was important, because it will undoubtedly help you understand what Semaxanib (SU5416) VEGFR2 inhibitor actually is. And, now we have come to that part. Basically, this small molecule drug was designed to block the activity of VEGFR2, which further leads to preventing VEGF from triggering the creation of new blood vessels, thus starving tumors and cutting off their supply lines.
How Does It Work?
Although the answer to this question should probably be clear to you already, let me share a quick and useful explanation about how Semaxanib (SU5416) VEGFR2 inhibitor works. Basically, it binds to the ATP-binding site of the VEGFR2 enzyme. Through taking the place of ATP, which is the molecule that provides energy for most cellular reactions, Semaxanib (SU5416) VEGFR2 inhibitor prevents this particular enzyme from transferring the signals. And, when the signaling chain is blocked, those tumor cells cannot divide or form new vessels.
Why Is It Important?
Why is Semaxanib (SU5416) VEGFR2 inhibitor so important, thought? Well, while it hasn’t really become a successful medicine for cancer treatment, this drug has definitely played a crucial role in proving that cutting off the blood supply could prevent a tumor from growing further. So, even though it didn’t see that great of a success, it undeniably paved the way to a lot of modern cancer therapies being developed.
To put it simply, Semaxanib (SU5416) VEGFR2 inhibitor changed the way scientists think about cancer, and about how to fight it. Previous treatments were mostly targeted at killing tumor cells directly. After the development of this drug, the focus has shifted, and scientists are now looking for, among other things, ways to cut off that blood supply, and thus attack the disease from a different angle. I suppose you understand how important that is, because it provides us with new treatment options.
