Biomaxx
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KY-19382
There has been some controversy over me posting this, and I want to clarify that under no circumstances will any compound sources and dosage advice be discussed. This is purely mechanistic and for high iq users only.
KY-19382 has been on the rise recently and whilst it is still a relatively unknown compound, im going to explain it to yall
pathway breakdown
KY-19382 runs through the CNP-NPR-B axis, this has effects downstream, dampening MAPK. This causes slower bone resorption and osteoclastogenesis, creating the ideal environment for osteoblast.
To pair with this it increaseses calcium and phosphate absorption and phosphate retention, this along with its CREB activation (bmp-2 signalling and osteocalcin expression) directly upregulates osteoblast.
-----------
The same cnp axis I mentioned is active in epiphyseal chondrocyte, so what does this mean for the growth plates?
delayed differentiation, hypertrophy and ossification.
this happens through 3 pathways-
PKG-11
FGF23
NPR-C/IHH
PKG-11
CNP binding indirectly activates cGMP surges which directly leads to heavy PKG-11 upregulation.
PKG-II phosphorylates
(SOX9,VASP,ROCK) suppress the chondrocyte transformation into a hypertrophic stage, alter cell adhesion and delay differentiation
FGF23
NPR-B directly suppresses FGF23
Lower FGF23=lower FGFR3
FGFR3 is fairly popular im sure you know how it works but ill give a lil analogy
Think of FGFR3 like border control
And growth signals are like the immigrants trying to cross the border (growth plates )
Less border control (FGFR3)
more immigrants (growth signals)
This allows more growth and also delays differentiation and ossification
NPR-C/IHH
KY-19382 reduces NPR-C count, NPR-C is what clears CNP. So less NPR-C means a longer CNP half life and stronger binding affinity. This CNP effect also modulates the IHH-PTHRP feedback loop.
IHH drives PTHRP to suppress differentiation and keep chondrocytes proliferating. CNP basically reinforces this.
--------------------------
KY-19382 upregualtes cGMP
cGMP upregulation causes increased blood flow to metabolically active tissue, this means there is a large increase in nutrition delivery, so more calcium, phosphates and amino acids to support bone remodeling. More nutrient delivery to osteoblast/clast. Also enhanced recovery in soft tissue
cGMP also modulates collagen synthesis. PKG activation in fibroblasts upregulates type I and type II collagen through CREB and SP1 activation, while increasing oxidase activity for better cross linking. This means denser bone, stronger connective tissue, and improved skin quality and faster hair growth.
------------
Fun fact- KY-19382 can make your eyes appear purple during usage
Sorry
birthdefect and
Fram3Let I hope I didnt leak too much
Ik this is a big change from my usual tone but I thought id prove my knowledge and more of my threads will be like this.
There really isnt alot of studies on this compound, im going of self taught and knowledge gathered from many others and some subscription ai research.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8251890/ -from
MirinZygos Ty
There has been some controversy over me posting this, and I want to clarify that under no circumstances will any compound sources and dosage advice be discussed. This is purely mechanistic and for high iq users only.
KY-19382 has been on the rise recently and whilst it is still a relatively unknown compound, im going to explain it to yall
pathway breakdown
KY-19382 runs through the CNP-NPR-B axis, this has effects downstream, dampening MAPK. This causes slower bone resorption and osteoclastogenesis, creating the ideal environment for osteoblast.
To pair with this it increaseses calcium and phosphate absorption and phosphate retention, this along with its CREB activation (bmp-2 signalling and osteocalcin expression) directly upregulates osteoblast.
-----------
The same cnp axis I mentioned is active in epiphyseal chondrocyte, so what does this mean for the growth plates?
delayed differentiation, hypertrophy and ossification.
this happens through 3 pathways-
PKG-11
FGF23
NPR-C/IHH
PKG-11
CNP binding indirectly activates cGMP surges which directly leads to heavy PKG-11 upregulation.
PKG-II phosphorylates
(SOX9,VASP,ROCK) suppress the chondrocyte transformation into a hypertrophic stage, alter cell adhesion and delay differentiation
FGF23
NPR-B directly suppresses FGF23
Lower FGF23=lower FGFR3
FGFR3 is fairly popular im sure you know how it works but ill give a lil analogy
Think of FGFR3 like border control
And growth signals are like the immigrants trying to cross the border (growth plates )
Less border control (FGFR3)
more immigrants (growth signals)
This allows more growth and also delays differentiation and ossification
NPR-C/IHH
KY-19382 reduces NPR-C count, NPR-C is what clears CNP. So less NPR-C means a longer CNP half life and stronger binding affinity. This CNP effect also modulates the IHH-PTHRP feedback loop.
IHH drives PTHRP to suppress differentiation and keep chondrocytes proliferating. CNP basically reinforces this.
--------------------------
KY-19382 upregualtes cGMP
cGMP upregulation causes increased blood flow to metabolically active tissue, this means there is a large increase in nutrition delivery, so more calcium, phosphates and amino acids to support bone remodeling. More nutrient delivery to osteoblast/clast. Also enhanced recovery in soft tissue
cGMP also modulates collagen synthesis. PKG activation in fibroblasts upregulates type I and type II collagen through CREB and SP1 activation, while increasing oxidase activity for better cross linking. This means denser bone, stronger connective tissue, and improved skin quality and faster hair growth.
------------
Fun fact- KY-19382 can make your eyes appear purple during usage
Sorry
birthdefect and
Fram3Let I hope I didnt leak too muchIk this is a big change from my usual tone but I thought id prove my knowledge and more of my threads will be like this.
There really isnt alot of studies on this compound, im going of self taught and knowledge gathered from many others and some subscription ai research.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8251890/ -from
MirinZygos Ty
Until next timebiomaxx
Last edited:
