Our proprietary and novel small-molecule pre-clinical programs, including TEM1657, have showed great efficacy, orally and topically, to remit psoriasis symptoms but without the common side effects associated with existing treatments
Inflammatory symptoms are rapidly reduced after the first application of our lead compounds, including TEM1657, in line with existing topical and oral treatments
Complete remission of psoriasis symptoms
No erythema – Regulated desquamation – Normal skin thickness
Greater efficacy than existing oral treatments (Apremilast)
Similar efficacy than existing topical corticosteroid treatments
Best-in class safety profile
No skin thinning (unlike corticosteroids), no observed side effect on animals in toxicity tests
No common side effects associated with existing topical and oral treatments
In separate pre-clinical models, a topical application of TEM1657 proved very efficacious, with rapid improvements after the first application. In 4 days, the healing process is as efficient as with existing corticosteroid treatment Dermoval (containing 0.05% Clobetasol).
The advantage of TEM1657 over corticosteroids is that, additionally to its efficacy, it preserves skin structure integrity and does not trigger skin atrophy.
In ongoing pre-clinical studies, a systemic administration of TEM1657 efficiently alleviated psoriasis symptoms, namely erythema, skin induration, and desquamation. In 7 days, the skin is healthy.
Pre-clinical efficacy is greater than existing oral treatment Apremilast with none of the associated common side effects.
What is Psoriasis?
Psoriasis is a relapsing and remitting inflammatory disease that affects skin and sometimes nails and joints. It has an overall prevalence of about 2% of the world’s population, with important geographical variation that may be attributed to differences in climate, genetic background and antigen exposure.
Psoriasis can take many different forms. The most prevalent form is plaque psoriasis, which is being characterized by skin patches with intense desquamation and loosely adherent silvery-white scales and affects mostly the elbows, knees, lower back, buttocks, and scalp. Less common forms include guttate psoriasis, pustular forms, erythrodermic psoriasis, and lichenified hands.
Skin lesions are due to the dysregulation of immune mediators, leading to hyperproliferation and aberrant differentiation of epidermal cells, increased dermal vascularity, and massive infiltration of immune cells. Involved immune mediators include IL-17, IL-23, IL-20, IL-22, IL-1β, IL-6, and TNF-α, which interact as a network in the pathogenesis of psoriasis.
Although the inflammation associated with psoriasis is generally limited to the skin, it can also progress to the joints causing psoriatic arthritis. Population studies have shown that about a third of patients develop psoriatic arthritis.Severe forms of psoriasis have also been associated with serious co-morbidities such as cardiovascular disease, Crohn’s disease, type II diabetes mellitus, obesity, dyslipidemia, the metabolic syndrome and lymphoma.
How it works
The Th17/23 axis is a natural warning signal delivered by certain immune cells that triggers immunity in case of pathogen infection with bacteria and fungi in the body. When abnormally activated or for too long after pathogen removal, the Th17/23 axis leads to chronic inflammation and generates autoimmune pathologies such as psoriasis.
This mechanism is common to other chronic inflammatory diseases such as rheumatoid arthritis, ankylosing spondylitis, Crohn’s disease, multiple sclerosis, vasculitis and atherosclerosis, lung disorders, asthma, and chronic obstructive pulmonary disease.
Temisis’s lead compounds, including TEM1657, have shown early-stage efficacy in modulating the activity of the Th17/23 axis, which explains in turn positive pre-clinical results as a treatment of psoriasis.
Ability to modulate the Th17/23 axis opens vast and exciting possibilities to use our compounds as potential treatments for numerous inflammatory diseases, beyond psoriasis.