Puberty stack, hightmax

[ineedhghsorces]

• 10ius of hgh (before bed)
  • Shown that low ius of hgh in adolescents with normal hgh production doesn't do anything but raise ur E2, so 10ius is needed
• 17.5 mgs of infigratinib every three days
  • Inhibits FGFR3
  • Three days due to its super-long half-life
• .25 mg of Arimidex every other day
  • Lowers Estrogen

Questions
Heard about Fulvestrant, have done much reasearch wondering if anyone is on it or knows a lot about it?
What's the deal with test during puberty? I'm somewhat new to this, so I have done much research on test or really any gear (besides hgh)?

 

[sln]

doesn't do anything but raise ur E2

I'm so sick of hearing this ngl

 

[ineedhghsorces]

I'm so sick of hearing this ngl

it ovy does stuff, but it's so little, yes, it will make you stronger, but for height, next to nothing

 

[sub5bhai]

raise ur E2

and what studies back this up

 

[sln]

it ovy does stuff, but it's so little, yes, it will make you stronger, but for height, next to nothing

That's untrue, even "low dose hgh" is miles better than natural production.

 

[ineedhghsorces]

That's untrue, even "low dose hgh" is miles better than natural production

Miles is a stretch, it helps for everything but hight. Thats why im taking 10ius

 

[sln]

Miles is a stretch, it helps for everything but hight. Thats why im taking 10ius

It's not a stretch by any means. Clearly you aren't educated on HGH well enough to be arguing on behalf of it.

 

[Lauren de Graaf]

Where

• 10ius of hgh (before bed)
  • Shown that low ius of hgh in adolescents with normal hgh production doesn't do anything but raise ur E2, so 10ius is needed
• 17.5 mgs of infigratinib every three days
  • Inhibits FGFR3
  • Three days due to its super-long half-life
• .25 mg of Arimidex every other day
  • Lowers Estrogen

Questions
Heard about Fulvestrant, have done much reasearch wondering if anyone is on it or knows a lot about it?
What's the deal with test during puberty? I'm somewhat new to this, so I have done much research on test or really any gear (besides hgh)

Where on earth did you source FGFR inhibitors from

 

[ineedhghsorces]

Where

Where on earth did you source FGFR inhibitors from

lmao, it took me a min, but I found a legit guy on tele

 

[itssoover0457]

whats the max dose of hgh u should take? i never heard of infigratinib where do i get it? i tjought only hgh and ai were needed for height growth. i heard steroids help too if side effects are managed. what are all the compounds u should take for maxxing ever mm of bone development

 

[itssoover0457]

lmao, it took me a min, but I found a legit guy on tele

send link

 

[ineedhghsorces]

It's not a stretch by any means. Clearly you aren't educated on HGH well enough to be arguing on behalf of it.

Only thing ive studied hgh for is height and its side effects, therefore why I'm taking 10ius. All I want it hight, so its other postive effects I don't really care about.

 

[ineedhghsorces]

whats the max dose of hgh u should take? i never heard of infigratinib where do i get it? i tjought only hgh and ai were needed for height growth. i heard steroids help too if side effects are managed. what are all the compounds u should take for maxxing ever mm of bone development

depends on ur weight 140-150 8-10ius

 

[itssoover0457]

depends on ur weight 140-150 8-10ius

i never heard of these other drugs. i thought u only needed hgh and ai. if i take every steroid and compound under the sun would each stack up and make me even taller? never heard of infigratinib. where do u source it

 

[ineedhghsorces]

and what studies back this up

Do any research on hgh and this will be brought up. E2 converts hgh into igf-1, therefore with more hgh more E2. https://pubmed.ncbi.nlm.nih.gov/15506073/.

 

[sub5bhai]

Do any research on hgh and this will be brought up. E2 converts hgh into igf-1, therefore with more hgh more E2. https://pubmed.ncbi.nlm.nih.gov/15506073/.

higher hgh ≠ higher e2, high estrogen can influence hgh not vice versa.

 

[ineedhghsorces]

higher hgh ≠ higher e2, high estrogen can influence hgh not vice versa.

I used the wrong link mb both of them where blue when i googled it, and i clicked the first one. You have to read the documents https://www.sciencedirect.com/science/article/pii/S0015028216586889


"Result(s): Follicle-stimulating hormone injection increased E2 and E2:T stimulated area under the curve (AUC) with respect to saline administration. Moreover, the E2 secretion wasincreased significantly in the group treated with GH plus FSH as compared with that found inthe group receiving FSH alone. Growth hormone itself was unable to increase any steroidogenicresponse by ovary in terms of both E2 and E2:T AUC values."

 

[sub5bhai]

I used the wrong link mb both of them where blue when i googled it, and i clicked the first one. You have to read the documents https://www.sciencedirect.com/science/article/pii/S0015028216586889


"Result(s): Follicle-stimulating hormone injection increased E2 and E2:T stimulated area under the curve (AUC) with respect to saline administration. Moreover, the E2 secretion wasincreased significantly in the group treated with GH plus FSH as compared with that found inthe group receiving FSH alone. Growth hormone itself was unable to increase any steroidogenicresponse by ovary in terms of both E2 and E2:T AUC values."

males don’t have ovaries that study was done on women

 

[mavJJ]

Larpstack lol

You wont do this

 

[holygreymacias]

I'm so sick of hearing this ngl

real

 

[Sayan.xdd]

• 10ius of hgh (before bed)
  • Shown that low ius of hgh in adolescents with normal hgh production doesn't do anything but raise ur E2, so 10ius is needed
• 17.5 mgs of infigratinib every three days
  • Inhibits FGFR3
  • Three days due to its super-long half-life
• .25 mg of Arimidex every other day
  • Lowers Estrogen

Questions
Heard about Fulvestrant, have done much reasearch wondering if anyone is on it or knows a lot about it?
What's the deal with test during puberty? I'm somewhat new to this, so I have done much research on test or really any gear (besides hgh)?

you're not getting your hand on infigratinib

 

[ineedhghsorces]

you're not getting your hand on infigratinib

you need my tele seller?

 

[Sayan.xdd]

i sent u a dm

 

[manuel355335]

lmao, it took me a min, but I found a legit guy on tele

Is it the guy with the core profile picture

 

[manuel355335]

• 10ius of hgh (before bed)
  • Shown that low ius of hgh in adolescents with normal hgh production doesn't do anything but raise ur E2, so 10ius is needed
• 17.5 mgs of infigratinib every three days
  • Inhibits FGFR3
  • Three days due to its super-long half-life
• .25 mg of Arimidex every other day
  • Lowers Estrogen

Questions
Heard about Fulvestrant, have done much reasearch wondering if anyone is on it or knows a lot about it?
What's the deal with test during puberty? I'm somewhat new to this, so I have done much research on test or really any gear (besides hgh)?

Are you doing this stack already?

 

[juttislife]

you need my tele seller?

Pm me, I can’t pm

 

[ineedhghsorces]

Are you doing this stack already?

yeah been like 2 and a half weeks no issues im monitoring everything. Lips/skin get dry and im kinda bloated but thats all

 

[TakaTeo]

• 10ius of hgh (before bed)
  • Shown that low ius of hgh in adolescents with normal hgh production doesn't do anything but raise ur E2, so 10ius is needed
• 17.5 mgs of infigratinib every three days
  • Inhibits FGFR3
  • Three days due to its super-long half-life
• .25 mg of Arimidex every other day
  • Lowers Estrogen

Questions
Heard about Fulvestrant, have done much reasearch wondering if anyone is on it or knows a lot about it?
What's the deal with test during puberty? I'm somewhat new to this, so I have done much research on test or really any gear (besides hgh)?

Explain why you feel you should use FGFR3s

do you guys understand how these things work?
Ask yourself some questions and try answer them before considering usage:

What does FGFR3 actually do in a normal skeleton?

Do you know what FGFR3 is doing in your growth plate right now, at baseline in the body?

Do you understand the Mutation specificity issues?

What is your FGFR3 activity level?

Do you understand what FGFR3 suppression actually produces?

Do you know what happens to growth plate architecture when FGFR3 is suppressed in a normal animal?

Do you know what FGFR1 does in the growth plate?

And finally in regards to infigratinib, do you know why it was withdrawn?

I would personally find it very intriguing to get the chance to know some of you who use FGFR3 inhibitors and other fun oncology drugs alongside massive amounts of growth enhancers, as I'm sure I'll have some fantastic research subjects to dissect when shit inevitably goes Cronenberg.

Fulvestrant is essentially a hydrogen bomb for your estrogen system. It is a SERD aka selective estrogen receptor degrader - this means that it will nuke the receptor entirely. Every tissue that uses the estrogen receptor from your desired bones, to clearly needed brain tissues, cardiovascular endothelium, even liver loses estrogen signalling simultaneously and COMPLETELY. That is not a dial or switch to be flipped it is a circuit breaker, for a postmenopausal woman breast cancer patient in late stage treatments where the alternative is death via disease progression, so it is acceptable.

 

[ineedhghsorces]

Explain why you feel you should use FGFR3s

do you guys understand how these things work?
Ask yourself some questions and try answer them before considering usage:

What does FGFR3 actually do in a normal skeleton?

Do you know what FGFR3 is doing in your growth plate right now, at baseline in the body?

Do you understand the Mutation specificity issues?

What is your FGFR3 activity level?

Do you understand what FGFR3 suppression actually produces?

Do you know what happens to growth plate architecture when FGFR3 is suppressed in a normal animal?

Do you know what FGFR1 does in the growth plate?

And finally in regards to infigratinib, do you know why it was withdrawn?

I would personally find it very intriguing to get the chance to know some of you who use FGFR3 inhibitors and other fun oncology drugs alongside massive amounts of growth enhancers, as I'm sure I'll have some fantastic research subjects to dissect when shit inevitably goes Cronenberg.

Fulvestrant is essentially a hydrogen bomb for your estrogen system. It is a SERD aka selective estrogen receptor degrader - this means that it will nuke the receptor entirely. Every tissue that uses the estrogen receptor from your desired bones, to clearly needed brain tissues, cardiovascular endothelium, even liver loses estrogen signalling simultaneously and COMPLETELY. That is not a dial or switch to be flipped it is a circuit breaker, for a postmenopausal woman breast cancer patient in late stage treatments where the alternative is death via disease progression, so it is acceptab

Great reposnce and thread. I took a break from homework and ima just write this quickly, ive done some research. Ik im not answering everything, but simply FGFR3 is just a break on bone growth telling cartilage cells to slow down their dividing. Not all FGFR3 mutations are equal, with achondroplasia being a partially stuck brake while thanatophoric dysplasia is a fully stuck one, meaning treatments need to be carefully calibrated to the specific mutation. Suppressing FGFR3 sounds like an obvious fix but is dangerous because it also disrupts related receptors like FGFR1 that are essential for blood vessel growth into bone and normal skeletal development. Infigratinib was withdrawn because it was too blunt a tool, hitting all FGFR receptors indiscriminately rather than precisely targeting just the overactive FGFR3, it does cause serious side effects like retinal toxicity but we really only see these in cancer doses. I get my blood work done monthly, i didnt read this over because I need to get back to my homework. If ur gonna respond, please give good valid info, not some bullshit

 

[ineedhghsorces]

Explain why you feel you should use FGFR3s

do you guys understand how these things work?
Ask yourself some questions and try answer them before considering usage:

What does FGFR3 actually do in a normal skeleton?

Do you know what FGFR3 is doing in your growth plate right now, at baseline in the body?

Do you understand the Mutation specificity issues?

What is your FGFR3 activity level?

Do you understand what FGFR3 suppression actually produces?

Do you know what happens to growth plate architecture when FGFR3 is suppressed in a normal animal?

Do you know what FGFR1 does in the growth plate?

And finally in regards to infigratinib, do you know why it was withdrawn?

I would personally find it very intriguing to get the chance to know some of you who use FGFR3 inhibitors and other fun oncology drugs alongside massive amounts of growth enhancers, as I'm sure I'll have some fantastic research subjects to dissect when shit inevitably goes Cronenberg.

Fulvestrant is essentially a hydrogen bomb for your estrogen system. It is a SERD aka selective estrogen receptor degrader - this means that it will nuke the receptor entirely. Every tissue that uses the estrogen receptor from your desired bones, to clearly needed brain tissues, cardiovascular endothelium, even liver loses estrogen signalling simultaneously and COMPLETELY. That is not a dial or switch to be flipped it is a circuit breaker, for a postmenopausal woman breast cancer patient in late stage treatments where the alternative is death via disease progression, so it is acceptable.

I saw sum bs tt about Fulvestrant, posted this, then read about it and understood how retarted it is

 

[TakaTeo]

Great reposnce and thread. I took a break from homework and ima just write this quickly, ive done some research. Ik im not answering everything, but simply FGFR3 is just a break on bone growth telling cartilage cells to slow down their dividing. Not all FGFR3 mutations are equal, with achondroplasia being a partially stuck brake while thanatophoric dysplasia is a fully stuck one, meaning treatments need to be carefully calibrated to the specific mutation. Suppressing FGFR3 sounds like an obvious fix but is dangerous because it also disrupts related receptors like FGFR1 that are essential for blood vessel growth into bone and normal skeletal development. Infigratinib was withdrawn because it was too blunt a tool, hitting all FGFR receptors indiscriminately rather than precisely targeting just the overactive FGFR3, it does cause serious side effects like retinal toxicity but we really only see these in cancer doses. I get my blood work done monthly, i didnt read this over because I need to get back to my homework. If ur gonna respond, please give good valid info, not some bullshit

Hello, I am off to bed but I assure you my line of questioning is not bullshit. - when you have the time in the near future and/or I have woken up and sent a more detailed reply, I recommend you look through the questions I asked in more detail, for example, I am not restating general concerns about FGFR3s, I am asking you to look into the actual mechanism of action behind these pathways in the body.

Inhibiting FGFR1 alongside FGFR3 is simultaneously suppressing the negative regulator of proliferation and the positive regulator of the differentiation that produces actual bone lengthening

Do you know where in the growth plate itself FGFR1 is specifically expressed; not in the vasculature, but in the chondrocytes themselves, and in which zone?

will return to read this again in the morning

 

[ineedhghsorces]

Hello, I am off to bed but I assure you my line of questioning is not bullshit. - when you have the time in the near future and/or I have woken up and sent a more detailed reply, I recommend you look through the questions I asked in more detail, for example, I am not restating general concerns about FGFR3s, I am asking you to look into the actual mechanism of action behind these pathways in the body.

Inhibiting FGFR1 alongside FGFR3 is simultaneously suppressing the negative regulator of proliferation and the positive regulator of the differentiation that produces actual bone lengthening

Do you know where in the growth plate itself FGFR1 is specifically expressed; not in the vasculature, but in the chondrocytes themselves, and in which zone?

will return to read this again in the morning

Alr another break from the hw. (its an essay thats why im taking breaks not that you care). Thanks for the real repsonce not just being a jackass. Off the top of my head I belive its the hypertrophic zone and hypertrophic chrondecytes, im not %100 sure tho. This is where cartilage is replaced by bone.

and if you inhibit FGFR3 and FGFR1 simultaneously, you are releasing the proliferation brake while simultaneously blocking the differentiation signal that converts cartilage into actual lengthened bone — you get cells dividing but not properly converting, which is architecturally chaotic rather than therapeutically useful.

Because of my time constraints (its a lot of work to put philosphy is an English essay) I wont be answers why I use them. But simply too much of anything is bad, but these smaller doses do more good than harm. I also find it funny on tt when u see Greys (im a Grey as well but yk) talking about FgFr-3 inhibitors. With not knowing anything. Infrgrib is the one i use beacuse I sorced it. If I find somthing that is better than I will.

 

[non omnis moriar]

• 10ius of hgh (before bed)
  • Shown that low ius of hgh in adolescents with normal hgh production doesn't do anything but raise ur E2, so 10ius is needed
• 17.5 mgs of infigratinib every three days
  • Inhibits FGFR3
  • Three days due to its super-long half-life
• .25 mg of Arimidex every other day
  • Lowers Estrogen

Questions
Heard about Fulvestrant, have done much reasearch wondering if anyone is on it or knows a lot about it?
What's the deal with test during puberty? I'm somewhat new to this, so I have done much research on test or really any gear (besides hgh)?

Low iq

 

[unknownhtnfromeu]

I'm so sick of hearing this ngl

so what range iu is the best then

 

[sln]

so what range iu is the best then

6-10

 

[unknownhtnfromeu]

6-10

i dotn have money for that much is there any point in doing a 3iu cycle?

 

[MintyFr]

you need my tele seller?

yo can u send me I have a infrig source but wanna see if urs cheaper also 3 days a bit long no? infrig half life is like 30 hours

 

[ineedhghsorces]

yo can u send me I have a infrig source but wanna see if urs cheaper also 3 days a bit long no? infrig half life is like 30 hours

yeah i agree 3 days is long, but with fgfr1-2 also being effected imo its better