Phase 1 Trial of Amnion Cell Therapy for Ischemic Stroke

You'll have to ask your doctor and stroke hospital to followup.  They have never done it in the past, so why would they start now?
https://www.frontiersin.org/articles/10.3389/fneur.2018.00198/full?

Thanh G. Phan¹*, Henry Ma¹, Rebecca Lim², Christopher G. Sobey³ and Euan M. Wallace²

• ¹Clinical Trials, Imaging and Informatics (CTI) Division, Stroke & Ageing Research (STARC), Department of Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, VIC, Australia
• ²The Ritchie Centre, Department of Obstetrics and Gynaecology, Hudson Institute of Medical Research, Monash Health and Monash University, Melbourne, VIC, Australia
• ³Department of Physiology, Anatomy and Microbiology, School of Life Sciences, LaTrobe University, Melbourne, VIC, Australia

Background: There is increasing interest in stem cell therapy as another treatment modality in stroke, particularly for patients who are unable to receive endovascular clot retrieval or thrombolysis therapies, or for whom standard treatment has failed. We have recently shown that human amniotic epithelial cells (hAECs) are effective in reducing infarct volume in different animal models of ischemic stroke, including in non-human primates. hAEC therapy attenuated infarct growth and/or promoted functional recovery, even when administered 1–3 days after the onset of stroke.

Methods: We now propose an open label Phase 1 dose escalation trial to assess the safety of allogeneic hAECs in stroke patients with a view to providing an evidence platform for future Phase 2 efficacy trials. We propose a modified 3 + 3 dose escalation study design with additional components for measuring magnetic resonance signal of efficacy as well as the effect of hAECs on immunosuppression after stroke.

Result: The trial will commence in 2018. The findings will be published in a peer-reviewed journal.

Conclusion: The trial is registered with ANZCTR (ACTRN12618000076279p).

Introduction

Prior to 2015, the standard clinical approach for reducing disability and death in ischemic stroke was Stroke Unit admission, antiplatelet therapy, and treatment with recombinant tissue plasminogen activator (TPA), within 4.5 h from onset in selected patients (1). However, the rate of vessel re-opening when there is a large obstructive clot is low (12%), even with TPA (2). Since 2015, there has been considerable optimism about the place of endovascular clot retrieval (ECR), for large clot removal, as a new and transformative therapy (1). However, even with this extended time window (up to 24 h), the number of eligible patients for ECR is less than 15% (1, 3). Further, a substantial proportion of those patients in the trial who received these treatments was left with moderate to severe disability or died (72% of patients who received TPA and 48% of those who received TPA and ECR) (2). In short, there remain enormous challenges in achieving the effective management of stroke across all patients. There is thus an urgent need to explore alternative therapeutic strategies that may be both suitable for more stroke patients and be more effective in improving outcome after stroke.

One such strategy is to move from the current time-based approach to an imaging tissue-based approach where treatment is based on the presence of salvageable ischemic tissue (3, 4). However, reperfusion therapies shift the peri-infarct zone toward the ischemic core but do not address the local and systemic immune response cascades that separate from the ischemic insult itself, promoting further tissue damage surrounding the infarct (5). The body’s intended effect of post-stroke immunosuppression appears to be the dampening of the “autoaggressive” Th1 immune response within the brain (6), but the unintended consequence is an increased risk of infection such as pneumonia (7), and this phenomenon is associated with high mortality and poor functional outcomes. These infiltrating inflammatory cells are located in the peri-infarct area, which has been referred to as the “inflammatory penumbra,” which denotes an area susceptible to further injury from the inflammatory cascade (5). Recognition of the need to manage the inflammatory response as part of stroke therapy has led to a call for future therapies that also focus on mitigating injurious events in the peri-infarct zone and not just on reperfusion therapy (5). In this regard, stem cell therapy has emerged as one potentially attractive option because of its ability to modulate inflammatory pathways at multiple sites appropriate to the changing pathophysiological state over time (8). By contrast, an example of a unimodal neuroprotectant drug target that would be unsuitable for modulating the inflammatory cascade is matrix metalloproteinase (MMP-9). In the early phase of stroke, MMP-9 damages the blood–brain barrier (BBB) (9) and contributes to vasogenic edema, whereas in later stages, it contributes to remodeling around the peri-infarct areas, and consequently targeting MMP-9 at this time can be harmful (5).

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