About us
Rinnerva is a biotechnological startup developing a groundbreaking new treatment for amyotrophic lateral sclerosis (ALS)
Our solution was developed following years of studying the basic mechanisms of the disease and joins three main concepts:
Targeting hallmark pathology
TDP-43 aggregates are shared among more than 97% of ALS patients. Rinnerva’s lead compound ‘G3-P1’ targets and dissolves TDP-43 aggregates.
Delivering to peripheral
nervous system
The most sensitive segment of the motor neuron is outside the central nervous system. Rinnerva delivers ‘G3-P1’ also to the peripheral nerves and neuromuscular junctions.
Focused on early intervention
We are confident that delivering our highly-potent treatment at an early time point of the disease can significantly halt the deterioration of patients and restore lost function.
The Rinnerva team
Israel-US experienced and excellence—driven team of neuroscientists and neurologist

Dr. Amir Dori
M.D., Ph.D.
CMO
Head of the Neuromuscular clinic at Sheba Tel HaShomer medical center, Israel

Prof. Jeffery L. Twiss
M.D., Ph.D.
President and Chairman of the board
Head of the neural repair and nerve regeneration research group, center for Childhood Neurotherapeutics, University of South Carolina

Dr. Ariel Ionescu
Ph.D.
COO
Entrepreneur
Expert in neuromuscular biology

Prof. Eran Perlson
Ph.D.
CSO
Head of the molecular neurodegeneration research group at the faculty of medicine, Tel-Aviv University

Dr. Pabitra Sahoo
Ph.D.
CTO
Head of the Molecular neurobiology research group at Rutgers University.
Our technology
G3-P1 is a proprietary peptide developed by Rinnerva toward clinical trials in Amyotrophic Lateral Sclerosis patients.
We are currently performing pre-clinical studies to determine the effective dose and administration paradigm as well as, to ensure the safety of G3-P1.
Targeting hallmark pathology
TDP-43 aggregates

TDP-43 aggregates are a key pathology observed in over 97% of ALS patients. Others and our prior studies have identified the presence and accumulation of TDP-43 aggregates in peripheral nerves at early timepoints in the disease – underlining the importance in targeting this pathology by early intervention.
Mechanism-targeting treatment
Rinnerva’s G3-P1 targets TDP-43 aggregates

Our lead product ‘G3-P1’ mimics one of TDP-43’s interactors in the aggregates, a protein called G3BP1, and thus serves as a decoy of TDP-43.
‘G3-P1’ interferes with TDP-43’s ability to target its cellular victims and form aggregates.
Known mode of action
G3-P1 dissolves
TDP-43 aggregates

Rinnerva’s G3-P1 not only blocks the formation of aggregates, but also interacts with existing pathological aggregates and dissolves those.
Dismantling of TDP-43 aggregates facilitates recovery of vital cellular functions, and so enables recovery of the motor unit.

Rinnerva is evolving
For more details, fill the form, or contact us via email.
Derech HaHadarim 7,
Ganei Tiqwa, IL
ariel@xals.io
(+972) 54 6296611

