ALTB-168 is a humanized therapeutic antibody with a unique mechanism of action, which preferentially induces down regulation of late-stage, chronically activated T cells. As a consequence, the treatment of ALTB-168 can lead to amelioration of multiple T-cell-driven autoimmunity and inflammation, including psoriasis,psoriatic arthritis,ulcerative colitis
Psoriasis is a complex, chronic relapsing and inflammatory skin disorder affecting 2-3% of the general population worldwide. Psoriasis vulgaris (chronic plaque psoriasis), the most common type of psoriasis, primarily features dry, sharply demarcated, raised erythematous skin plaques covered by silvery scales. Cumulated evidence suggested that dysfunctional helper T cells (Th1, Th17, Th22, and Treg cells) are indispensable factors in psoriasis development.
Two phase 2 studies with ALTB-168 were completed. In both studies ALTB-168 demonstrated signs of clinical efficacy in patients with moderate to severe chronic plaque psoriasis.
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Psoriatic arthritis (PsA) is a clinically heterogeneous chronic inflammatory disease, comprising a range of musculoskeletal (joints, nails, and entheses) and dermatological manifestations associated with impaired physical function and poor quality of life. Evidence supports that T cells plays a vital role in initiating and substantiating psoriatic arthritis by generating inflammatory cytokines which stimulate the attraction of inflammatory cells to the synovium and joint tissues, resulting in the deterioration of cartilage and bone.
Indeed, a phase 2a study with ALTB-168 was completed. From 15 PsA patients completing 7 courses of ALTB-168 treatment, significant improvement was seen in 8 patients at week 12 (primary endpoint), with some responders maintaining significant efficacy through week 24.
These encouraging results will now need confirmation in an appropriate Phase II trial with a suitable target population and expanded number of patients.
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Ulcerative colitis (UC), characterized by the hallmark clinical symptoms of bloody diarrhea, rectal urgency, and tenesmus, is a chronic inflammatory disease affecting the colorectal mucosa. The underlying pathogenesis of UC is complex, and accumulating evidence suggests that environmental factors contribute to triggering an overly active or dysregulated T-cell mediated immune-inflammatory response in genetically predisposed individuals, which eventually leads to mucosa damage.
Phase 2a anti-TNF α and/or anti-integrin refractory/intolerant Ulcerative Colitis trial has been completed, with signs of clinical efficacy demonstrated. Continued UC development is planned with ALTB-268.
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