Therapeutic antibody MNAC13

Top view of the antigen binding region of the MNAC13 monoclonal antibody: when MNAC13 binds the TrkA receptor, it prevents it from being activated by nerve growth factor.

There is a growing body of evidence indicating Nerve Growth Factor (NGF) and its high-affinity receptor TrkA as important mediators in inflammatory pain states: NGF levels increase in inflammed tissue and NGF neutralization prevents inflammation-related hyperalgesia.

MNAC13 is a humanized anti-TrkA antibody with function neutralising properties which make it a unique tool to contrast pathological situation characterized by hyperfunction of the NGF/TrkA system.

MNAC13 displays remarkable analgesic properties in several animal models of persistent pain.
It has a surprising long-lasting effect in the CCI model, in which two phases can be distinguished in the action of MNAC13: the first one (including the treatment period and the first week following the end of treatment itself) identifies a pharmacological effect of MNAC13; the second phase identifies a long-term effect of MNAC13, which likely involves new gene expression and characterizes MNAC13 as a disease-modifying drug, a feature that is actually unique in the field of neuropathic pain.
MNAC13 displays a remarkable synergistic effect when co-administered with doses of other analgesic drugs that are not efficacious per se.

These results have important implications in view of the therapeutic use of the antibody: in fact, the possibility of reaching a significant analgesic effect with a limited number of antibody administrations and the possibility of significantly lowering the dose of other currently used analgesic drugs, thanks to co-administration of MNAC13, would both have a tremendous impact in terms of clinical application.

MNAC13 humanized antibody has been recently licensed-out to a pharmaceutical company partner who will develop it for untreatable forms of chronic and inflammatory pain.

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