TY - JOUR
T1 - Clinical development of passive tau-based immunotherapeutics for treating primary and secondary tauopathies
AU - Panza, Francesco
AU - Dibello, Vittorio
AU - Sardone, Rodolfo
AU - Castellana, Fabio
AU - Zupo, Roberta
AU - Lampignano, Luisa
AU - Bortone, Ilaria
AU - Stallone, Roberta
AU - Cirillo, Nicoletta
AU - Damiani, Christian
AU - Altamura, Mario
AU - Bellomo, Antonello
AU - Daniele, Antonio
AU - Solfrizzi, Vincenzo
AU - Lozupone, Madia
PY - 2023
Y1 - 2023
N2 - IntroductionTauopathies are clinicopathological entities with increased and pathological deposition in glia and/or neurons of hyperphosphorylated aggregates of the microtubule-binding protein tau. In secondary tauopathies, i.e. Alzheimer's disease (AD), tau deposition can be observed, but tau coexists with another protein (amyloid-& beta;). In the last 20 years, little progress has been made in developing disease-modifying drugs for primary and secondary tauopathies and available symptomatic drugs have limited efficacy.Areas coveredThe present review summarized recent advances about the development and challenges in treatments for primary and secondary tauopathies, with a focus on passive tau-based immunotherapy.Expert opinionSeveral tau-targeted passive immunotherapeutics are in development for treating tauopathies. At present, 14 anti-tau antibodies have entered clinical trials, and 9 of them are still in clinical testing for progressive supranuclear palsy syndrome and AD (semorinemab, bepranemab, E2814, JNJ-63733657, Lu AF87908, APNmAb005, MK-2214, PNT00, and PRX005). However, none of these nine agents have reached Phase III. The most advanced anti-tau monoclonal antibody for treating AD is semorinemab, while bepranemab is the only anti-tau monoclonal antibody still in clinical testing for treating progressive supranuclear palsy syndrome. Further evidence on passive immunotherapeutics for treating primary and secondary tauopathies will come from ongoing Phase I/II trials.
AB - IntroductionTauopathies are clinicopathological entities with increased and pathological deposition in glia and/or neurons of hyperphosphorylated aggregates of the microtubule-binding protein tau. In secondary tauopathies, i.e. Alzheimer's disease (AD), tau deposition can be observed, but tau coexists with another protein (amyloid-& beta;). In the last 20 years, little progress has been made in developing disease-modifying drugs for primary and secondary tauopathies and available symptomatic drugs have limited efficacy.Areas coveredThe present review summarized recent advances about the development and challenges in treatments for primary and secondary tauopathies, with a focus on passive tau-based immunotherapy.Expert opinionSeveral tau-targeted passive immunotherapeutics are in development for treating tauopathies. At present, 14 anti-tau antibodies have entered clinical trials, and 9 of them are still in clinical testing for progressive supranuclear palsy syndrome and AD (semorinemab, bepranemab, E2814, JNJ-63733657, Lu AF87908, APNmAb005, MK-2214, PNT00, and PRX005). However, none of these nine agents have reached Phase III. The most advanced anti-tau monoclonal antibody for treating AD is semorinemab, while bepranemab is the only anti-tau monoclonal antibody still in clinical testing for treating progressive supranuclear palsy syndrome. Further evidence on passive immunotherapeutics for treating primary and secondary tauopathies will come from ongoing Phase I/II trials.
KW - Alzheimer’s disease
KW - FTLD-Tau
KW - PSPS
KW - tauopathies
KW - mild cognitive impairment
KW - monoclonal antibodies
KW - tau
KW - dementia
KW - Alzheimer’s disease
KW - FTLD-Tau
KW - PSPS
KW - tauopathies
KW - mild cognitive impairment
KW - monoclonal antibodies
KW - tau
KW - dementia
UR - http://hdl.handle.net/10807/257990
U2 - 10.1080/13543784.2023.2233892
DO - 10.1080/13543784.2023.2233892
M3 - Article
SN - 1354-3784
VL - 32
SP - 625
EP - 634
JO - Expert Opinion on Investigational Drugs
JF - Expert Opinion on Investigational Drugs
ER -