Sarah is having a heart attack. What happens in the next hour will determine if she survives – and the quality of the rest of her life.
Breakthrough Therapy
If Sarah had the option to receive earlier intervention in the ambulance following a 911 call, or in the ER, there could be an opportunity to reduce the risks to her clinical prognosis. That is why IMMEDIATE is developing IMT-358. FDA has designated IMT-358 as a Breakthrough Therapy for the treatment of acute coronary syndrome to reduce the risk of mortality, hospitalization for heart failure, and cardiac arrest.
IMT-358: Program Overview
Metabolic stabilization during the earliest phase of acute ischemia
The Unaddressed Window in Acute Ischemia
Acute ischemic events trigger rapid metabolic collapse at the cellular level, initiating a cascade of injury that becomes irreversible within minutes.
While current standards of care prioritize restoring blood flow, they do not address the underlying metabolic failure that develops during the earliest phase of ischemia—when tissue remains salvageable but unprotected.
IMT-358 was designed to address this critical gap by stabilizing cellular metabolism during this time-sensitive window, with the goal of preserving tissue viability and reducing downstream injury.
What IMT-358 Is Designed to Do
IMT-358 is a novel metabolic stabilization therapy intended for administration at the point of care in emergency settings, including pre-hospital and early in-hospital environments.
By supporting cellular energy balance during acute ischemic stress, IMT-358 is designed to interrupt the cascade of injury that leads to infarction, arrhythmia, and tissue loss.
The program is grounded in decades of translational research and clinical investigation into metabolic modulation in ischemic heart disease.
Current Standard of Care
Current standards of care for acute ischemic events are designed to restore blood flow, not to stabilize cellular metabolism.
Reperfusion therapies, antithrombotics, and supportive measures are typically initiated after patients reach definitive care settings and are focused on re-establishing circulation and preventing secondary injury. While these interventions are essential, they do not address the rapid metabolic collapse that begins within minutes of ischemic onset—during the interval when tissue remains viable but highly vulnerable.
As a result, a critical window exists between symptom onset and definitive reperfusion in which tissue fate is determined, yet no approved therapy is designed to protect or stabilize cellular metabolism during this phase.
What is IMT-358?
IMT-358 is an investigational drug under development by IMMEDIATE Therapeutics to provide metabolic protection, potentially to to minimize cardiac damage and instability during Acute Coronary Syndromes (ACS).
ACS manifests as chest pain or discomfort, shortness of breath, dizziness, nausea, sweating, and discomfort in left or both arms, the jaw, neck, back or stomach. At that point, immediate medical attention is needed.
IMT-358 Begins When Time is Most Critical
IMT-358 is designed for early administration during the initial phase of ischemia, bridging the critical period between symptom onset and definitive reperfusion, when myocardial tissue is ischemic but still salvageable.
In clinical studies, the therapy has been administered intravenously in pre-hospital and early in-hospital emergency settings, integrating seamlessly into existing ACS care pathways. Unlike current standards of care, which focus primarily on restoring coronary blood flow, IMT-358 targets the metabolic and inflammatory injury that develops during ischemia—before reperfusion can be achieved. By stabilizing myocardial metabolism during this critical window, IMT-358 is intended to complement reperfusion therapies and reduce downstream tissue damage, cardiac instability, and long-term complications.
IMT-358 targets the critical window before reperfusion, when cardiac tissue is still salvageable but unprotected.
How is IMT-358 believed to work
Acute coronary syndrome (ACS), either a heart attack or angina pectoris that can rapidly lead to a heart attack, is caused by insufficient blood flow to the heart muscle due to a clot (“thrombosis”) in a coronary artery. This causes heart muscle to be starved of oxygen and nutrients which causes cardiac instability that can lead to immediate cardiac arrest and causes permanent damage (infarction).
Modulating Metabolic Injury During Ischemia
During acute ischemia, reduced oxygen delivery limits oxidative metabolism, forcing myocardial cells to rely on alternative energy sources. This shift leads to rapid mobilization of free fatty acids (FFAs), which increases oxygen demand, promotes mitochondrial dysfunction, and activates inflammatory pathways. Elevated FFAs have been associated with worsening myocardial injury and infarct expansion. IMT-358 is believed to mitigate these effects by rapidly reducing circulating FFAs during ischemia, thereby moderating downstream inflammatory and metabolic injury. The precise mechanism of action continues to be evaluated.
IMMEDIATE-1 demonstrated rapid and sustained reduction in circulating FFAs following IMT-358 administration compared with placebo.
Clinical Foundation
The IMT-358 program is supported by clinical evidence from the NIH-funded IMMEDIATE-1 trial, a randomized study evaluating early intravenous metabolic therapy administered in the pre-hospital setting for patients with suspected acute coronary syndromes.
Clinical Evidence: IMMEDIATE-1 Trial
- Randomized, controlled NIH-funded trial
- Early administration during acute coronary syndromes
- Demonstrated reductions in infarct size, cardiac arrest, and mortality
Administration in Clinical Studies
In clinical studies, IMT-358 has been administered intravenously in emergency settings, including pre-hospital and early in-hospital care, during acute coronary syndromes. This administration strategy is intended to enable early metabolic intervention during ischemia, prior to or alongside standard reperfusion therapies.
Development Status
IMT-358 is advancing toward pivotal clinical development under an FDA-aligned regulatory strategy.
The program is supported by clinical evidence from the NIH-funded IMMEDIATE-1 trial and is progressing under a Special Protocol Assessment (SPA) that governs the planned pivotal development pathway. IMMEDIATE Therapeutics is preparing for a Phase 3 clinical program designed to support a Biologics License Application (BLA), with ongoing activities focused on regulatory readiness, manufacturing preparedness, and operational planning.
Broader Potential
IMT-358 is advancing under an FDA-aligned development strategy, supported by a Special Protocol Assessment (SPA) governing the planned pivotal program.
The program has also received Breakthrough Therapy Designation, reflecting the unmet medical need and the potential for meaningful clinical benefit.
IMMEDIATE Therapeutics is preparing for a pivotal Phase 3 program designed to support a Biologics License Application (BLA).
Regulatory Pathway
While IMT-358 is initially focused on acute coronary syndromes, the underlying biology of metabolic stabilization during ischemic stress has relevance across other acute and high-risk settings.
IMMEDIATE Therapeutics is intentionally advancing IMT-358 through a focused initial indication while preserving the opportunity to expand into additional ischemic contexts over time.
IMT-358 represents a fundamentally different approach to acute ischemic care—focused on timing, metabolic preservation, and early intervention.
The program is advancing toward pivotal development with a strong clinical foundation, regulatory alignment, and experienced leadership.
Published Research
- Selker HP et al. Effect of out-of-hospital administration of intravenous glucose, insulin, and potassium (GIK) in patients with suspected acute coronary syndromes: The IMMEDIATE randomized controlled trial. 2012;307(18):1925-1933. PMID 22452807.
- Grossman AN et al. Glucose-insulin-potassium revived: current status in acute coronary syndromes and the energy-depleted heart. 2013;127:1040-1048. PMID 23459576.
- Selker HP et al. Very Early Administration of Glucose-Insulin-Potassium (GIK) by Emergency Medical Service for Acute Coronary Syndromes: Biological Mechanisms for Benefit in the IMMEDIATE Trial. Amer Heart J. 2016;178:168–175. PMID 27502865.
- Selker HP et al. One-year outcomes of out-of-hospital administration of intravenous glucose, insulin and potassium (GIK) in patients with suspected acute coronary syndrome in the IMMEDIATE (Immediate Myocardial Metabolic Enhancement During Initial Assessment and Treatment in Emergency care) trial. Am J Cardiol. 2014;113(10):1599-605. PMID 24792735
- Stone GW et al. Relationship Between Infarct Size and Outcomes Following Primary PCI: Patient-Level Analysis From 10 Randomized Trials. J Am Coll Cardiol. 2016 Apr 12;67(14):1674-83. PMID: 27056772.
- Selker HP et al. Relationship Between Therapeutic Effects on Infarct Size in Acute Myocardial Infarction and Therapeutic effects on One-year Outcomes: A Patient-Level Analysis of Randomized Clinical Trials. Am Heart J. 2017 Jun;188:18-25. PMID 28577674.
- Beshansky JR et al. A community consultation survey to evaluate support for and success of the IMMEDIATE trial. Clinical Trials. 2014;11(2):178-186. PMID 24686107
- Sullivan AL et al. Factors associated with longer time to treatment for patients with suspected acute coronary syndromes. Circ Cardiovasc Qual Outcomes. 2014;7:86-95. PMID 24425697
- Ray M et al. A predictive model to identify patients with suspected acute coronary syndromes at high risk of cardiac arrest or in-hospital mortality: An IMMEDIATE Trial sub-study. Int J Cardiol Heart & Vasculature. 2015;9:37-42. PMID: 26913292
- Ellis KL, et al. Common variants associated with changes in levels of circulating free fatty acids after administration of glucose-insulin-potassium (GIK) therapy in the IMMEDIATE trial. Pharmacogenomics J. 2017 Jan;17(1):76-83. doi: 10.1038/tpj.2015.84. Epub 2015 Dec 8. PMID: 26644202.
Development Status
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IMMEDIATE-1 Phase 2 trial completed
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FDA alignment via Special Protocol Assessment
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Breakthrough Therapy Designation granted
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Phase 3 development planned