I AM ASSUMING YOU READ MY PREVIOUS POST AND KNOW THE PATHWAYS!!! Or no need just go to end and see simplified version
I do not have ANY qualification and do NOT take all of this just because i said so do your OWN research this is just a stepping stone
Any terms/words you dont know search them up or ask me and ill elaborate and edit the post to fix inconsistencies
https://looksmax.cc/threads/pathways-related-to-bone-growth.274/
compounds, what are they?
All of these compounds target previous pathways that i wrote about and i will explain more. They basically mimic/imitate shit
detailed explanations per compound
compound 1: teriparatide (forteo)
what it does/how it works: recombinant PTH(1-34) daily subQ mimics intermittent pulses in Ihh/PTHrP loop binding PTH1R on osteoblasts firing cAMP/PKA upregulating Runx2 cranking formation 2-3x 9-13% BMD gains. extends plate proliferation.cons: black-box osteosarcoma risk in rodents rare in humans hypercalcemia nausea max 2 years or rebound pricey $41K/year shots suck.
pathway it helps: mainly Ihh/PTHrP by delaying hypertrophy keeping proliferation active longer like the loop does also ties to wnt/β-catenin for osteoblast proliferation.
studies backing it up: a study showed teriparatide led to sustained lower incidences of vertebral hip and other fractures for up to 8 years after switching to antiresorptive agents proving long-term bone formation boost. (pubmed.ncbi.nlm.nih.gov ). another found it facilitates osteogenic diff of bone mesenchymal stem cells alleviating idiopathic osteoporosis via circFNDC3B-miR pathway tying to prolif. (link.springer.com ).
https://pubmed.ncbi.nlm.nih.gov/40054513/
“Overall, significant improvement was observed in pretreated and treatment-naïve patients undergoing teriparatide treatment.”
https://link.springer.com/article/10.1186/s12891-025-08505-2
“In summary, our study demonstrated that TPD treatment promoted osteogenic differentiation”
compound 2: abaloparatide (tymlos)
what it does/how it works: PTHrP analog daily subQ selective PTH1R agonist less resorption than teri upregulates osteoblast genes 11-18% BMD gains superior gains. stimulates plate prolif.cons: orthostatic hypotension hypercalcemia rodent osteosarcoma signal 2-year limit injections tedious.
pathway it helps: targets Ihh/PTHrP like PTHrP in the loop delaying hypertrophy boosting prolif also indirect wnt activation for net formation.
studies backing it up: a study showed abaloparatide increases bone formation without affecting growth of bone-disseminated cancer cells suggesting safe mass boost. (pubmed.ncbi.nlm.nih.gov ). another found local abaloparatide promotes alveolar bone augmentation in orthodontic models via regulating pathways and growth factors. (link.springer.com). By the way if you actually read all this use the word “crazy” in a reply im curious who reads this
https://pubmed.ncbi.nlm.nih.gov/40584157/
“These results suggest that abaloparatide may be effectively used to increase bone mass without stimulating growth of cancer cells”
https://link.springer.com/article/10.1186/s12903-025-06915-1
“The micro-CT results indicated that abaloparatide treatment significantly enhanced the percentage of bone, trabecular thickness, trabecular number, and bone surface density.”
compound 3: romosozumab (evenity)
what it does/how it works: sclerostin-inhibiting mAb monthly subQ blocks wnt inhibitor allowing β-catenin nuclear shift osteoblast prolif/diff dual builds bone slows resorption 13-15% BMD spike. rapid frame thickening plate extension potential.cons: CV risks heart attack/stroke black-box jaw necrosis rare rebound without follow-up.
pathway it helps: unlocks wnt/β-catenin by inhibiting sclerostin stabilizer for osteoblast prolif/diff high in hypertrophy zone.
studies backing it up: a study confirms romosozumab's dual mechanism increasing formation reducing resorption via wnt pathway. (pmc.ncbi.nlm.nih.go). another showed increase in serum DKK1 attenuates anabolic response proving wnt modulation. (academic.oup.com ).
https://pmc.ncbi.nlm.nih.gov/articles/PMC11955074/
“Results indicated that fused bone volume was significantly higher in the R group at the last observation of the fused bone. “
https://academic.oup.com/jbmr/advance-article/doi/10.1093/jbmr/zjaf110/8237915
“Romosozumab stimulates bone formation by inhibiting sclerostin”
compound 4: denosumab (prolia)
what it does/how it works: RANKL-inhibiting mAb every-6-month subQ halts osteoclast maturation net gain 8-10% BMD indirect anabolic preserving matrix.cons: hypocalcemia infections rebound fractures eczema spinal issues.
pathway it helps: blocks RANKL in resorption balance indirect help to formation pathways like wnt bmp by stopping breakdown.
studies backing it up: a study showed denosumab produces continuous BMD increase over ten years low fracture risk. (pmc.ncbi.nlm.nih.gov ). another on modulatory efficacy vs zoledronic acid in osteoporosis confirming safety bone metabolism modulation. (frontiersin.org ).
https://pmc.ncbi.nlm.nih.gov/articles/PMC11889064/
“Our findings suggested that abaloparatide treatment can link bone regeneration and ALP and BMP-2 levels in dose”
https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar..1666421/full
“After 1 year of treatment, BMD of lumbar spine significantly increased”
compound 5: vosoritide (voxzogo)
what it does/how it works: CNP analog daily/weekly subQ binds NPR-B raising cGMP/PKG inhibits FGFR3/ERK brake boosting prolif/hypertrophy +1-2cm/year in ACH. counters short stature off-label potential.cons: injection pain headaches BP drops long-term unknown non-ACH.
pathway it helps: amps CNP/NPR-B gas pedal opposing FGFR3 brake for more prolif delay hypertrophy.
studies backing it up: a study showed ongoing effects on adult height skeletal deformities quality of life in ACH. (pmc.ncbi.nlm.nih.gov ). another presented new data for vosoritide in achondroplasia via FGF signaling slowdown. (investors.biomarin.com ).
https://pmc.ncbi.nlm.nih.gov/articles/PMC12352272/
“with treated individuals growing an average of 1.5-2.0 cm/year faster than untreated peers”
https://investors.biomarin.com/news/news-details//BioMarin-Presents-New-Data-for-VOXZOGO-vosoritide-in-Children-with-Achondroplasia-and-Other-Skeletal-Conditions-at-Two-International-Endocrinology-Meetings/default.aspx (holy link nigga)
compound 6: YKL-05-099
what it does/how it works: SIK2/3 inhibitor oral blocks salt-inducible kinases boosting osteoblast activity trabecular mass no resorption spike. +12% density oral frame building.cons: mild GI CV safety TBD mostly preclinical.
pathway it helps: mimics PTH-like in Ihh/PTHrP uncoupling formation from resorption also ties to wnt.
studies backing it up: a 2024 study showed YKL-05-099 enhances fracture repair improved mechanical response later healing phases. (frontiersin.org 2024). another on dual targeting SIK CSF1R uncouples formation resorption via YKL-05-099. (elifesciences.org 2021 confirmed ongoing).
https://www.frontiersin.org/journal...logy/articles/10.3389/fbioe.2024.1450611/full
“ Furthermore, μCT analysis demonstrated increased mineralized bone volume”
https://elifesciences.org/articles/67772
“YKL-05–099 treatment increased trabecular bone mass in the femur and L5 vertebral body of hypogonadal female mice”
compound 7: compound 6641 (only if it was called 6741)
what it does/how it works: RXFP2 agonist oral relaxin mimic activates osteoblasts +20% BMD low-density models. oral booster height/density no tox preclin.cons: early stage off-target relaxin effects vascular.
pathway it helps: relaxin mimic for osteoblast prolif tying to IGF-1 wnt activation.
studies backing it up: a 2022 study discovered compound 6641 as RXFP2 agonist promoting bone formation in vivo pharmacokinetic fine-tune. (nature.com 2022). another on small molecule agonists RXFP2 for bone growth. (researchgate.net 2022 ongoing implications).
https://www.nature.com/articles/s42003-022-04143-9
“Optimized molecules displayed high potency and efficacy in the cAMP assay”
https://www.researchgate.net/public...ists_of_the_Relaxin_Family_Peptide_Receptor_2
“promoting osteoblast bone formation, both of which result in increased bone mass.“
compound 8: EB613
what it does/how it works: oral PTH(1-34) tablet gut-absorbed mimics teriparatide +2-4% BMD osteoblast stim. no shots height potential young.cons: GI tolerance phase 3 pending hypercalcemia risk.
pathway it helps: same as teriparatide Ihh/PTHrP loop via PTH1R for prolif delay hypertrophy.
studies backing it up: a phase 2 showed EB613 positive BMD effects trabecular cortical in postmenopausal women. (investors.enterabio.com ). another phase 2 6-month placebo-controlled met all biomarkers BMD endpoints safety. (investors.enterabio.com ).
https://investors.enterabio.com/new...ts-positive-effects-eb613-both-trabecular-and
“The improvements across multiple parameters, including integral volumetric BMD, cortical thickness, and cortical surface BMD, suggest that there is an early strengthening effect”
https://investors.enterabio.com/new...ents-positive-new-clinical-data-eb613-phase-2
“In early postmenopausal women (≤10 years since last menstrual period), EB613 (n=8) versus placebo (n=19), statistically significant BMD increases were observed at six months:”
compound 9: rhBMP-2
what it does/how it works: recombinant BMP-2 scaffolds local delivery binds BMPRs activating Smads Runx2 osteoinduction defects. regenerates bone fractures +vascularized volume.cons: inflammation ectopic bone high dose risks.
pathway it helps: direct BMP signaling for chondrocyte maturation Ihh expression hypertrophy ossification.
studies backing it up: a study showed rhBMP-2 coated BCP enhances early graft substitution socket preservation. (pmc.ncbi.nlm.nih.gov ). another optimizes rhBMP-2 for bone regeneration via signaling mechanisms. (mdpi.com ).
https://pmc.ncbi.nlm.nih.gov/articles/PMC12087511/
“At 3 months, BMP and non‐BMP groups had 3.17% and 3.12% new bone formation, respectively, and 3.8% and 37.85% of residual grafts”
https://www.mdpi.com/1422-0067/26/21/10723
“it possesses a strong capacity to stimulate bone formation.”
pros and cons lists per compound (for maxxing context)
Obviously all of these build bones for more specififics on how much check the studies i linked and the shit in advanced overviewteriparatide (forteo):
- pros: huge BMD spikes height extension well-studied.
- cons: cancer risk daily shots short-term only.
- pros: good BMD gains 11-18% less sides than teri bone-safe cancer models.
- cons: rodent cancer signal hypotensive.
- pros: dual build/slow rapid monthly ease also big bmd spike 13-15%.
- cons: heart risks necrosis rebound.
- pros: long-lasting 6 months density gains 8-10%.
- cons: rebound fractures hypoCa infections.
- pros: +2cm proven and up to 11cm extra compared to untreated opposes FGFR3.
- cons: shots hurt BP sides ACH-specific.
- pros: oral anabolic healer no resorption, +12% density preclinical.
- cons: GI mild early CV unknown.
- pros: oral density no tox relaxin mimic. +20% bmd
- cons: vascular possible phase 1 only.
- pros: oral PTH gains like injectables compliance. +2-4 bmd
- cons: GI Ca spikes ongoing trials.
- Pros: powerful local direct bmp signalling regens defects targeted.
- cons: ectopic/inflam dose dangers.
Once again thanks for reading i request you ask me to fix things which arnt clear or ask questions. btw alot of BMD gain wont necessarily mean it will be visible. visible will be less noticeable ur bones will jsut be thicker. however if ur a kid and growth plates open then visible changes more likely and more noticeable. pls do own research and contribute and give compound names u have heard of so i can add or write ab
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