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Scientific Background

FHL-401 is an intranasal peptide inhibitor of the MYD88-TLR2 interaction with a potent anti-inflammatory function. FHL-401 targets Alzheimer’s Disease (AD) and Rheumatoid Arthritis (RA) with a unique mechanism of action not present in other treatments.


FHL-201 specifically blocks the TLR2 signaling pathway which is implicated in the pathogenesis of AD and RA. FHL-201 improved short-term, long-term, and spatial memory in preclinical animal models for AD. Furthermore, in collagen-induced animal models for RA, it significantly reduced inflammation, enhanced locomotor activity and improved footprint behavior. Thus, FHL-201 is shown to be a good drug candidate for treating AD and RA patients.


Alzheimer’s disease is the most common neurodegenerative disorder in the elderly. Rheumatoid Arthritis is an autoimmune disease which is marked by inflammation and pain in joints. No effective treatment is currently available to cure or halt the progression of these diseases. The amyloid cascade hypothesis is widely accepted as one of the underlying pathogenic causes. There is a huge unmet need to find treatments for AD due to the increasing aging population.


During the early stage of AD, β-Amyloid aggregates are known to interact with TLR22 to enhance microglial Aβ uptake, effectively cleaning up Aβ plaques. However, as the disease progresses, the same interaction with TLR2 starts to activate microglia to induce inflammatory responses. The attenuation of microglial activation by inhibiting TLR2 promises to be a logical therapeutic approach for treating AD. Unfortunately, there is no direct inhibitor of TLR2.  Consequently, FHL-201, a novel peptide corresponding to the TLR2-interacting domain of MyD88 (TIDM) is designed to circumvent such disease progression.