Epigel (TP7193) in Joint Diseases

While Joint Diseases lack efficient pharmacologic treatments, TP7193 is an emerging, short-acting DMOAD candidate and tendon-repair therapeutic. 
epi list3.png


  • Joint Diseases Osteoarthritis (OA) and Tendinopathies(TP) are traumatic or age-related, widespread, poorly-met medical needs.

  • TP7193 is candidate disease-modifying OA drug (DMOAD) and tendinosis therapeutic with projected positive clinical outcomes in 3 to 4 weeks.

  • TP7193 is first-in-class epigenetic drug for Joint Diseases. In preliminary case series it produced remission in OA and TP (where just symptomatic medications are available) after limited non-cumulative applications.

  • TP7193 is a metabolic drug endowed of high safety, MOS (NOAEL/SED) ≈170; and fast clearance, Cmax<24h after single dose. 

  • By transdermal route, TP7193 reaches a local therapeutic level of 3-8 μM prospecting a domiciliary treatment, i.e. without injection and/or the administration within hospital premises.

  • Fast-track development by clinical entry via Medical Device may bypass the inertial lag-time of classic Rx drugs. 

  • Search for funding will consolidate a Spin-out pursuing potent high-value  therapeutics, where co-development on selected targets is also envisaged. 

  • The project aim at complete Proof-of-Concept studies in relevant indications, Knee OA, DDD and Elbow-Shoulder (ES) tendinosis.


Options in Osteoarthritis (OA) and tendinopathies are pharmacologic, non-pharmacologic therapies and combinations.

Hyaluronic acid (HA) or corticosteroids (CS) intra-articular are considered the effective interventions, yet with expected relapse. 

NSAIDs still dominate the arthropathy arena despite limited efficacy, for example acetaminophen has provided evidences of lack of effectiveness. 

Moreover, anti-pain opioids are now shunned because of the epidemic of addiction and the recognition that opioids are not a valid pain relief option in OA patients with an active lifestyle. 


Despite a large therapeutic armamentarium, over the last 5 years the quest for successful disease modifying OA drugs (DMOADs) remains substantial.

Recent DMOAD trials  encompass chondroprotective factors and drugs targeting inflammatory cytokines, signaling mediators, senescence, and pain. Yet, antibodies against inflammatory mediators like IL-1 and TNF-α failed in recent OA clinical trials. 

Although repurposed Osteoporosis drugs show compelling results in pre-clinical testing in OA, clinical trials in late-stage OA, such as multiple phase III trials investigating calcitonin, not yet demonstrated obvious benefits. (e.g. Galcanezumab). 

Beside research into surgical and cell-based strategies, the framework of principles applicable to chondroprotective or chondrogenetic approaches, means the DMOAD trials. 


TP7193 is an emerging disease-modifying OA drug (DMOAD) and TP therapeutic by fast-acting (2-4 weeks) in discontinuous dose.

TP7193 at 4-8 μM concentration promotes the Sox 9 expression and homeostasis of the chondrocyte phenotype. 

A controlled dosage of TP7193 pivots the differentiation and expansion. Higher doses shall induce terminal differentiation via Runx2/3, β catenin and Osteix, causing endochondral ossification.