Date: 2017-03-20
Type of
information: Publication of results in a medical journal
phase: preclinical
Announcement: publication of results in PNAS
Company: Syntimmune (USA - MA)
Product: SYNT002
Action
mechanism:
Disease:
Therapeutic
area:
Country:
Trial
details:
Latest
news:
- • On March 20, 2017, Syntimmune announced the peer-reviewed publication of research findings for SYNT002, its second most advanced pipeline program and lead monoclonal antibody therapy targeting albumin-FcRn interactions. SYNT002 is in active preclinical development by Syntimmune for a number of indications and is expected to enter IND-enabling studies in 2017. The study, led by Syntimmune scientific founder Dr. Richard Blumberg in collaboration with multiple members of the Company’s Scientific Advisory Board, appears in the journal Proceedings of the National Academy of Sciences (doi: 10.1073/pnas.1618291114 PNAS March 20, 2017). These research findings demonstrate that inhibition of FcRn (neonatal Fc receptor) provides protection against toxin-induced liver injury and causes removal of toxins from circulation via a newly described mechanism that is engaged by SYNT002. Among the key results are:
- While FcRn in the liver maintains albumin homeostasis, inhibition of albumin-FcRn binding caused clearance of albumin from the circulation via transport into the bile.
- Using acetaminophen poisoning as a preclinical model of an albumin-bound hepatotoxin, FcRn inhibition was shown to increase albumin-mediated transport of acetaminophen out of the circulation and into the bile where it is excreted from the body, protecting the liver and other organs from this toxin.
- In addition to inducing sequestration of albumin-bound toxins in bile, FcRn blockade caused albumin accumulation within hepatocytes, exerting important anti-oxidant effects to protect liver cells from acetaminophen damage.
- Multiple therapeutic modalities, including SYNT002 and a peptide mimetic inhibitor of FcRn, engaged this mechanism to provide robust protection from acetaminophen-induced liver toxicity
Is
general: Yes
