d-jnki-1 and Cochlear-Diseases

There is a growing interest in the auditory community to develop novel prophylactic and therapeutic drugs to prevent permanent sensorineural hearing loss following acute cochlear injury. The jun-N-terminal protein kinase (JNK) pathway plays a crucial role in acute sensory hearing loss. Blocking the JNK pathway using the cell-penetrating peptide D-JNKI-1 (AM-111/brimapitide) has shown promise as both a prophylactic and therapeutic agent for acute cochlear injury. A number of pre-clinical and clinical studies have determined the impact of D-JNKI-1 on acute sensorineural hearing loss. Given the inner-ear selective therapeutic profile, local route of administration, and ability to diffuse across cellular membranes rapidly using both active and passive transport makes D-JNK-1 a promising oto-protective drug. In this review article, we discuss the application of D-JNKI-1 in various auditory disorders as well as its pharmacological properties and distribution in the cochlea.

Topics: Animals; Cell Membrane Permeability; Cell-Penetrating Peptides; Cochlea; Cochlear Diseases; Cytoprotection; Enzyme Inhibitors; Hearing; Hearing Loss, Sensorineural; Humans; JNK Mitogen-Activated Protein Kinases; Peptides; Prognosis; Risk Factors; Signal Transduction