It took my savings and 14 years but I’m about to beat arthritis

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It is an absurd headline but having to take a drug for life is surely better than the pain of arthritis.

> enables the regeneration of affected tissues

This needs some heavy scrutiny, it seems like this is related to tanezumab. Which yes, blocks pain by affectively sticking a lego in front of another lego that when connected says hey I'm hurt, but doesn't pro-actively heal anything as far as I'm aware.

The usual play with claims like this is that with reduced inflammation there might be a better chance of circulation allowing for better natural regeneration (somewhat true?). But active regeneration of damaged tissue especially in places typically afflicted with athritis is a bit more complex because it's often at osteochondral boundry layers aren't as vascularized.

"it restores protective processes to diseased joints and enables the regeneration of affected tissues. It works by blocking a compound that supports the nerve cells involved in transmitting pain signals to the brain."

Yes, I guess you could belittle that by calling it 'a painkiller'. No different at all to taking a handful of ibuprofen, which every arthritis sufferer knows enables regeneration and why it is a solved problem.

My only commentary would be that these results do not read like clinical success, but rather something suggesting they should move on to phase III clinical trials.

This is the only publication I found in a quick search:

https://pubmed.ncbi.nlm.nih.gov/37976118/

>> Abstract

Objectives: Nerve growth factor β (β-NGF) is a protein which is important to the development of neurons particularly those involved in the transmission of pain and is central to the experience of pain in osteoarthritis (OA). Direct NGF antagonism has been shown to reduce OA pain but is associated with rapidly progressive OA. The aim of the study is to investigate the ability of soluble neurotrophin receptors in the NGF pathway to modulate pain in OA.

Methods: Synovial fluid (SF) was obtained from the knee joints of 43 subjects who underwent total knee arthroplasty. Visual analogue scale (VAS) pain scores were obtained prior to surgery. Customised-automated-ELISAs and commercial-ELISAs and LEGENDplex™ were used to measure soluble low-affinity nerve growth factor (LNGFR), soluble tropomyosin receptor kinase (TrkA), proNGF, β-NGF, other neurotrophins (NT) and cytokines including inflammatory marker TNF-α.

Results: The VAS score positively correlated with β-NGF (r=0.34) and there was positive association trend with neurotrophin-3 (NT-3), BDNF and negative association trend with ProNGF. sLNGFR positively correlated with VAS (r=0.33). The β-NGF/soluble TrkA ratio showed a strong positive correlation with VAS (r=0.80). In contrast, there was no correlation between pain and the β-NGF/sLNGFR ratio (r=-0.08). TNF-α positively correlated with β-NGF (r=0.83), NT-3 (r=0.66), and brain-derived neurotrophic factor (BDNF) (r=0.50) and negatively with ProNGF (r= -0.74) and positively correlated with both soluble TrkA (r=0.62), sLNGFR (r=0.26).

Conclusions: This study suggests that endogenous or cleaved sLNGFR, but not soluble TrkA may participate in OA pain modulation thus supporting further research into soluble LNGFR as a therapeutic target in OA.