neooni
Member
Recently I've been getting more and more into height biology and I've stumbled upon something that I find quite interesting (anyone that has the slightest clue about height growth biology probably already knows this :feelswhy
when I learned about the IHH (and thus HH pathway) and looked into the importancy of it regarding height and sceletal growth, I thought of ways to maybe stimulate it more than intented (kinda like stimulating the igf-1 axis with hgh) and then came across SAGs (Smoothened agonists). And thought maybe its something that we could use to our advantage?
How they work:
So you all know the HH (Hedgehog) pathway. In simple terms it works by binding to its receptor; PTCH(1) -> activating SMOs and so on. SAGs remove the whole PTCH step and stimulate the HH pathway more efficiently due to PTCH serving as a kind of body programmed brake to prevent overstimulating the hedgehog pathway. Thus sags keeps SMO continuously on leading to a longer lasting signaling.
The MAIN problem as of todays knowledge:
1. [BIGGEST PROBLEM] Overstimulating of IHH (thus HH) leads to brain- and skincancer and birth defects (when the kid in the womb has a hh defect). I mean, skin cancer is highly treatable. But who wants to have brain cancer growing FAST and often undetected? Not me atleast. And its the opposite of gh which grows tumors when theyre already there, this one LEADS TO the tumors.
2. Probably near impossible to source, since the majority of HH / IHH studies are done with their respective inhibitors, Smoothened agonists are not as often used. Sourcing Smoothened Agonists is harder than for some tiktokcels to find a simple gh source:lul: Even if we research them more and find ways to prevent certain types of cancer from them, sourcing them on grey markets will be near impossible.
Let me know if any of you guys is educated in this topic and put your thoughts below! Sadly I'm still a low iq individual compared to a lot of people here:feelsuhh:
How they work:
So you all know the HH (Hedgehog) pathway. In simple terms it works by binding to its receptor; PTCH(1) -> activating SMOs and so on. SAGs remove the whole PTCH step and stimulate the HH pathway more efficiently due to PTCH serving as a kind of body programmed brake to prevent overstimulating the hedgehog pathway. Thus sags keeps SMO continuously on leading to a longer lasting signaling.
The MAIN problem as of todays knowledge:
1. [BIGGEST PROBLEM] Overstimulating of IHH (thus HH) leads to brain- and skincancer and birth defects (when the kid in the womb has a hh defect). I mean, skin cancer is highly treatable. But who wants to have brain cancer growing FAST and often undetected? Not me atleast. And its the opposite of gh which grows tumors when theyre already there, this one LEADS TO the tumors.
2. Probably near impossible to source, since the majority of HH / IHH studies are done with their respective inhibitors, Smoothened agonists are not as often used. Sourcing Smoothened Agonists is harder than for some tiktokcels to find a simple gh source:lul: Even if we research them more and find ways to prevent certain types of cancer from them, sourcing them on grey markets will be near impossible.
Let me know if any of you guys is educated in this topic and put your thoughts below! Sadly I'm still a low iq individual compared to a lot of people here:feelsuhh: