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In today’s vid I’ll be speaking about a synergistic effects of 2 cheep and easy to access and administrate compounds that can be used to maximise ur runx2 output for appositional growth benefits.
Brotezobim:
What is Brotezobim ( brotz) .
Brotz is a proteasome inhibitor used to treat multiple myeloma (mm) where cancer cells highjack the bone remodeling process’s causing excess bone loss and reabsorption while also slowing down bone formation. MM does this thru many ways but the most pronounced ways it interfered with bone remodeling is via Increse of sots and dkk1. Brotz has been proven to decrease dkk1 and sots by up to 50% each ( systemic levels ) in some models proving it’s a powerful inhibitor of these wnt antagonists. Brotz has also been shown to Inhbit ostoclast formation and activity by inhibiting RANKL via the prevention of breaking down IKb what then would lock and prevent any NF-kB from causing production of RANKL. Brotz also prevents the break down of many anabolic bone growth genes such as b catetin, runX2 and Sp7, thus forcing osteoblast count activity to spike and increasing bone formation rates.
Fingolimod:
What is fingolimod ( fing ) ?
Fing is an oral medication that’s used to treat relapsing remitting multiple sclerosis and its main function is acting as a S1P modulator preventing auto agresive lymphocytes from exiting lymph nodes into the cns. But it also has profound epigenetic effects on bone remodelling.
It’s bone remodelling effects are via increasing runx2 mRNA and SP7 mRNA expression as seen in this graph: ( look in files for pics sorry )
It does this by entering the cell ( ostoblast in this instance ) and then interfering with SphK2 in the nucleus this then converts fing ( also called FTY720 ) into its active form FTY720-P and once it’s been phosphorylated inside the cell it can bind to active sites of class hdac I and Inhbit thier enzymatic functions this keeping histones highly acetylated resulting in the up regulation of runx2 and Sp7.
Fing also down regulates osteoclast activity by up regulating hdac4 in ostoclast what then surpasses ATF4 a transcript factor crucial for ostoclast survival shitting down Nf-Kb preventing the ostoclast from maturing fully. This happens bc ostoclast have a lot of extracellular S1P receptors what then fing bings to ( this case we care about S1P1 ) receptor degrading it thus casing that surge in hdac4.
So why use them together:
The reason why these compounds have really good synergy so good that there’s even a study of using them together is because as I said brotz prevents the break down of runx2 and Sp7 while fing increases the mRNA substantially ( so much so that the castrated mice ended up having more mRNA of both of runx2 and Sp7 then sham while normally casteation leads to a 30-50% decrease in mRNA of runx2 and 50-70% decrease in mRNA of Sp7 while also decreasing APL by 60-80% and ONC by 50-80% where as fig even nearly kept them in the castrated model at around the same level as sham as seen in this graph:
Dosing:
Brotz: 1.75-2mg on days I will list and then followed by a 10 day break. Subq ( in belly fat administrated )
Days: 1-4-8-11 then 10 days break repeat and remember to take the 10 day break or you’ll be casing more harm then good
Fing: 0.5-0.75 mg a day that’s it and it’s oral
Also I wanted to add that Brotz has this side effect called Chemotherapy-Induced Peripheral Neuropathy that can cause major pain but it’s been show that fing fully prevents this from happening so ye just a cool fact ig.
Ok thanks for reading and remember join dc in my bio and if u have questions ping my user ( methylated_0 ) my 19nor_abuse account is limited on dc oki i love you all byeeee . 
( TikTok is 19nor_abuse )
Also brotz is 10-20 usd per 2.5 mg and fing is 15-20 usd for 0.5x28 pills India mart both oki bye
Brotezobim:
What is Brotezobim ( brotz) .
Brotz is a proteasome inhibitor used to treat multiple myeloma (mm) where cancer cells highjack the bone remodeling process’s causing excess bone loss and reabsorption while also slowing down bone formation. MM does this thru many ways but the most pronounced ways it interfered with bone remodeling is via Increse of sots and dkk1. Brotz has been proven to decrease dkk1 and sots by up to 50% each ( systemic levels ) in some models proving it’s a powerful inhibitor of these wnt antagonists. Brotz has also been shown to Inhbit ostoclast formation and activity by inhibiting RANKL via the prevention of breaking down IKb what then would lock and prevent any NF-kB from causing production of RANKL. Brotz also prevents the break down of many anabolic bone growth genes such as b catetin, runX2 and Sp7, thus forcing osteoblast count activity to spike and increasing bone formation rates.
Fingolimod:
What is fingolimod ( fing ) ?
Fing is an oral medication that’s used to treat relapsing remitting multiple sclerosis and its main function is acting as a S1P modulator preventing auto agresive lymphocytes from exiting lymph nodes into the cns. But it also has profound epigenetic effects on bone remodelling.
It’s bone remodelling effects are via increasing runx2 mRNA and SP7 mRNA expression as seen in this graph: ( look in files for pics sorry )
It does this by entering the cell ( ostoblast in this instance ) and then interfering with SphK2 in the nucleus this then converts fing ( also called FTY720 ) into its active form FTY720-P and once it’s been phosphorylated inside the cell it can bind to active sites of class hdac I and Inhbit thier enzymatic functions this keeping histones highly acetylated resulting in the up regulation of runx2 and Sp7.
Fing also down regulates osteoclast activity by up regulating hdac4 in ostoclast what then surpasses ATF4 a transcript factor crucial for ostoclast survival shitting down Nf-Kb preventing the ostoclast from maturing fully. This happens bc ostoclast have a lot of extracellular S1P receptors what then fing bings to ( this case we care about S1P1 ) receptor degrading it thus casing that surge in hdac4.
So why use them together:
The reason why these compounds have really good synergy so good that there’s even a study of using them together is because as I said brotz prevents the break down of runx2 and Sp7 while fing increases the mRNA substantially ( so much so that the castrated mice ended up having more mRNA of both of runx2 and Sp7 then sham while normally casteation leads to a 30-50% decrease in mRNA of runx2 and 50-70% decrease in mRNA of Sp7 while also decreasing APL by 60-80% and ONC by 50-80% where as fig even nearly kept them in the castrated model at around the same level as sham as seen in this graph:
Dosing:
Brotz: 1.75-2mg on days I will list and then followed by a 10 day break. Subq ( in belly fat administrated )
Days: 1-4-8-11 then 10 days break repeat and remember to take the 10 day break or you’ll be casing more harm then good
Fing: 0.5-0.75 mg a day that’s it and it’s oral
Also I wanted to add that Brotz has this side effect called Chemotherapy-Induced Peripheral Neuropathy that can cause major pain but it’s been show that fing fully prevents this from happening so ye just a cool fact ig.
Ok thanks for reading and remember join dc in my bio and if u have questions ping my user ( methylated_0 ) my 19nor_abuse account is limited on dc
oki i love you all byeeee . ( TikTok is 19nor_abuse ) Also brotz is 10-20 usd per 2.5 mg and fing is 15-20 usd for 0.5x28 pills India mart both oki bye
