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ForumsOther Peptides & Research CompoundsBPC-157 and tendon healing — September 2026

BPC-157 and tendon healing — September 2026

MeganSA_TX Wed, Jul 2, 2025 at 7:37 PM 27 replies 1,881 viewsPage 1 of 6
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MeganSA_TX
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Jul 2, 2025 at 7:37 PM#1

Putting this up for argument rather than for agreement. I have read it twice and I am still not certain what it supports.

The pharmacokinetics explain nearly every practical question asked here. Albumin binding above 99% slows clearance enough to make weekly dosing possible; a terminal half-life near a week means four to five weeks to steady state and therefore a four-week titration interval; subcutaneous bioavailability around 89% means injection site barely matters. Those three facts answer most timing questions before they are asked.

Where I think it is weakest: the comparator does most of the work in how this gets reported, and it is not the comparator most people think they are citing.

What would genuinely help is knowing which effects tachyphylax and which persist, because the answer explains why tolerability improves while the appetite effect keeps working. I have searched first, so if this is covered somewhere point me at it and I will read it.

Note on sourcing:
Figures above are from the primary publication rather than the press summary. If a number here disagrees with one you have, post yours and we will work out which of us is reading a secondary source.
10 5PharmD_Rodriguez, julia.endo, JessicaM_2024 and 7 others
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Dr.ObesityLA
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Jul 2, 2025 at 9:36 PM#2
MeganSA_TX said:
The pharmacokinetics explain nearly every practical question asked here.

Amycretin (AMY/GLP-1 dual agonist) emerging data relevant to the pharmacology: Phase 1 showed -13.1% body weight at only 12 weeks, the fastest trajectory ever seen for an anti-obesity agent[1].

Amylin receptor agonism enhances satiety signaling through the area postrema and reduces glucagon secretion. Combined with GLP-1R agonism, this dual mechanism may produce even greater efficacy than current agents.

Early-stage data — interpret with caution. But the trajectory is extraordinary.

References:
[1] Novo Nordisk investor presentation, September 2023.
Last edited: Jul 2, 2025 at 10:36 PM
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TrialNerd_Beth
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Jul 2, 2025 at 11:35 PM#3
MeganSA_TX said:
The pharmacokinetics explain nearly every practical question asked here.

This is where I part company with the consensus forming above. The mechanism is more central than most summaries suggest. Receptor agonism in the arcuate nucleus activates POMC neurons and inhibits AgRP/NPY signalling, and the downstream MC4R pathway is the same one disrupted in monogenic obesity — convergent genetic evidence that the target is the right one. Peripherally there is glucose-dependent insulin secretion, glucagon suppression and delayed gastric emptying, but the gastric component largely adapts over months while the central effect persists, which is why the durable effect is appetite rather than fullness.

Ask again with the specifics and you will get a better answer than this one.

Last edited: Jul 3, 2025 at 3:35 AM
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Dr.EndoIndy
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Jul 3, 2025 at 1:34 AM#4
TrialNerd_Beth said:
The mechanism is more central than most summaries suggest.

Semaglutide structural biology relevant to the pharmacology: semaglutide is a 31-amino acid peptide with 94% homology to native GLP-1(7-36). Three key modifications enable its pharmacokinetic profile:

  1. Aib8 substitution: DPP-4 resistance (prevents enzymatic degradation)
  2. Arg34 substitution: improved chemical stability
  3. C18 fatty diacid at Lys26: albumin binding → long half-life

These three modifications transform a peptide with a 2-minute half-life (native GLP-1) into one with a 168-hour half-life (semaglutide). A masterclass in peptide engineering.

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SandraNC_45
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Jul 3, 2025 at 1:17 PM#5
Dr.ObesityLA said:
Amycretin (AMY/GLP-1 dual agonist) emerging data relevant to the pharmacology: Phase 1 showed -13.1% body weight at only 12 weeks, the fastest…

Mine went the same way, slower.

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