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Kv2.1-Targeted First in Class Neuroprotective Therapeutic for Acute Ischemic Stroke

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R43NS127620-01A1
Agency Tracking Number: R43NS127620
Amount: $231,974.00
Phase: Phase I
Program: SBIR
Solicitation Topic Code: 105
Solicitation Number: PA21-259
Timeline
Solicitation Year: 2021
Award Year: 2023
Award Start Date (Proposal Award Date): 2023-09-20
Award End Date (Contract End Date): 2025-08-31
Small Business Information
CELDARA MEDICAL, LLC
Lebanon, NH 03766-1441
United States
DUNS: 828763263
HUBZone Owned: No
Woman Owned: No
Socially and Economically Disadvantaged: No
Principal Investigator
 JULIE COLEMAN
 (617) 320-8521
 jc@celdaramedical.com
Business Contact
 JAKE REDER
Phone: (617) 320-8521
Email: jr@celdaramedical.com
Research Institution
N/A
Abstract

Project Summary
Acute ischemic stroke (AIS) impacts 795,000 Americans per year, leaving 90% of patients with chronic disability.
Prevalent cases of AIS in the US were estimated at 6.7M in 2017, translating to 6M Americans living with
permanent stroke-related disability. AIS is characterized by cerebrovascular blockage that results in the
formation of a central infarct with a surrounding ischemic penumbra; the goal for neuroprotection is based on the
fundamental concept of penumbral preservation (a.k.a. penumbral freezing). Currently, the only approved
therapy for patients suffering from AIS is the thrombolytic agent alteplase (tPA), approved in 1996 and burdened
by expansive side effects, a host of contraindications restricting eligible patient populations, and a limited
therapeutic time window. Importantly, the use of mechanical thrombectomy has drastically increased in the past
decade, bringing along improved clinical outcomes. It has been strongly argued that thrombectomy outcomes
can be further improved by neuroprotective therapies that salvage neuronal loss in the penumbra. Our team has
identified a signaling pathway that is ubiquitously activated following ischemic injury, enabling the completion of
neuronal programmed cell death. Our lead neuroprotective, CM-EA1, specifically disrupts this neuronal cell
death pathway. CM-EA1 is being developed to treat patients suffering from AIS, to prevent neuronal loss in the
ischemic penumbra, translating to decreased disability-adjusted life years (DALYs) for patient suffering from AIS.
In this application, we will demonstrate efficacy via a rigorous rat transient middle cerebral artery occlusion
(tMCAO) dose-escalation study. Following these key efficacy studies, we will advance CM-EA1 to aged rodent
models and large gyrencephalic animals in a Phase II development program. Our multidisciplinary team brings
together a unique combination of academic, clinical and commercial expertise that will permit the development
of a life-changing drug for AIS patients.

* Information listed above is at the time of submission. *

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