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Iron
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do you have a source for ky-19382 as a cnp/npr agent?
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
Sorrybirthdefect 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.
View attachment 37607
View attachment 37608
Until next time
biomaxx
Did u not read the first fucking paragraphdo you have a source for ky-19382 as a cnp/npr agent?
Tysm , added
Did u not read the first fucking paragraph
dnr ill read later seems interesting because i saw Lewis talking abt purple eyesKY-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
Sorrybirthdefect 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/ -fromMirinZygos Ty
View attachment 37607
View attachment 37608
Until next time
biomaxx
Status- bumpedKY-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
Sorrybirthdefect 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/ -fromMirinZygos Ty
View attachment 37607
View attachment 37608
Until next time
biomaxx
YO NIGGA WTFKY-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
Sorrybirthdefect 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/ -fromMirinZygos Ty
View attachment 37607
View attachment 37608
Until next time
biomaxx
jfl even in this article it mentions the real moa which i wrote about in my thread
nooooo nigga actual cnp modulation does thatJust made me experience the Dunning-Kreuger effect first hand. Holy shit I have so much to learn. From what I gather, this molecule improves nutrient delivery to the chondrocytes while simultaneously preventing ossification? Seems to have a lot of potential. Love the analogy you used btw
Mirin hard, bump.
Nigga what ? Are u fr ?YO NIGGA WTF
did you use the wrong compoudn? not a single molecule is true
ky has literally nothing to do with cnp bro you gotta delete this deadass
and wdym it can make your eyes appear purple
i think i said that to you as a joke cus i wanted my eyes to turn purple, that shit is not happening tho sadly
broooo nigga this looks like it was written for a different compound, probably the biggest biomax blunder of all time
Shit, I js fucking stemmed of pathways. Fuck broYO NIGGA WTF
did you use the wrong compoudn? not a single molecule is true
ky has literally nothing to do with cnp bro you gotta delete this deadass
and wdym it can make your eyes appear purple
i think i said that to you as a joke cus i wanted my eyes to turn purple, that shit is not happening tho sadly
broooo nigga this looks like it was written for a different compound, probably the biggest biomax blunder of all time


wdym stemmed of?Shit, I js fucking stemmed of pathways. Fuck bro![]()
nah like literally nothing is correctCrazy shit man, I pretty much got its effects down is js used to completely wrong pathway ? I need to stop writing threads high fml
I acc do not know, it think I js started writing on cnp . Fml, sober day 1wdym stemmed of?
can you elab on what happened, genuinely curious
alr gl niggaI acc do not know, it think I js started writing on cnp . Fml, sober day 1
if you want you can use my thread as an encyclopedia, afaik everything in there is true
Fr I was confused the whole time reading the thread because I could’ve sworn it was used for hair growth and not bonesYO NIGGA WTF
did you use the wrong compoudn? not a single molecule is true
ky has literally nothing to do with cnp bro you gotta delete this deadass
and wdym it can make your eyes appear purple
i think i said that to you as a joke cus i wanted my eyes to turn purple, that shit is not happening tho sadly
broooo nigga this looks like it was written for a different compound, probably the biggest biomax blunder of all time
Icl I didn’t read the whole article I just saw it before and said he would’ve talked about itjfl even in this article it mentions the real moa which i wrote about in my thread
cxxc5 - dvl inhibition and gsk3b inhibition
for both actually, cxxc5 is highly expressed in both hair and the growth plateFr I was confused the whole time reading the thread because I could’ve sworn it was used for hair growth and not bones
this isnt the first time ive seen on here where people will link sources that they just dont readIcl I didn’t read the whole article I just saw it before and said he would’ve talked about it
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
Sorrybirthdefect 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/ -fromMirinZygos Ty
View attachment 37607
View attachment 37608
Until next time
biomaxx
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.


