Our COVID-19 Response Efforts

Caladrius is leveraging our cell therapy expertise and resources to help patients and communities fighting the COVID-19 pandemic. We believe we are uniquely positioned to contribute to the combat of this public health threat using our proprietary CD34+ cell technology to help repair COVID-19 induced lung damage and restore human health.


CLBS119 is Caladrius’ CD34+ cell therapy product candidate for COVID-19 survivors who are experiencing difficulty breathing (shortness of breath or hypoxia). The FDA has authorized administration of CLBS119 under its Expanded Access IND Guidelines to evaluate the safety and efficacy of autologous, peripheral-blood-derived CD34+ cells for repair of COVID-19-induced lung damage in adults who have recovered from the virus but require supplemental oxygen.

Human Coronavirus Disease 2019

In December 2019, when a new pneumonia-like illness in China was identified as “Coronavirus Disease 2019” (COVID-19), Caladrius moved quickly to determine whether our CD34+ cell technology could play a role in responding to the growing public health threat. COVID-19 is caused by the virus “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2). The extent of the disease, its epidemiology, pathophysiology and clinical manifestations are being well-documented on an ongoing basis (Guan et al. 2020; Yang et al. 2020).

Pulmonary injury is a principal cause of COVID-19 morbidity and mortality

One important feature of the COVID-19 infection is the predominance of pulmonary manifestations. To date, the reported fatalities have virtually all been accompanied by evidence of pneumonia and systemic inflammation (Zhou et al. 2020; Pan et al. 2020; Xu et al. 2020; Xie et al. 2020). In addition, anecdotal evidence indicates that attenuation of inflammation may be beneficial in COVID-19 pneumonia (Zhu et al. 2020).

Vascular endothelial damage appears to precipitate end-organ damage in COVID-19

Evidence is accumulating indicating that vascular endothelial injury may be a precipitating factor in severe organ damage caused by COVID (Varga et al. 2020). Varga et al found multiple examples of viral invasion of vascular endothelial cells associated with inflammation, endothelial cell death, microvascular dysfunction and organ failure. Tian et al identified evidence of vascular leakage in the lungs of COVID-19 patients (Tian et al. 2020) indicating a severe loss of vascular integrity. The authors also reported vascular congestion. In sum, the findings are consistent with inflammation and severe vascular damage.

Prior data from the SARS epidemic suggest that CD34+ cells in the lung could be a target of the COVID-19 infection and that destruction of lung CD34+ progenitors could account for the inability of patients with severe pulmonary manifestations to fully recover (Chen et al. 2007).

Evaluating our existing CD34+ Cell Technology for the Repair of COVID-19 Induced Lung Damage

CD34+ cells are well known as hematopoietic stem cells (Berenson et al. 1988). In 1997, Asahara et al. described another function of CD34+ cells as endothelial progenitor cells capable of inducing the formation of new vasculature (Asahara et al. 1997). This tissue repair capability was then documented in a variety of preclinical models (Taguchi et al. 2004; Kawamoto, Iwasaki, et al. 2006), leading to the clinical development of autologous CD34+ cell therapy in multiple indications. These clinical studies have yielded substantial evidence for safety and efficacy for reversal of tissue damage in humans (Kawamoto, Katayama, et al. 2006; Losordo et al. 2007; Kawamoto et al. 2009; Losordo et al. 2011; Losordo et al. 2012; Ohtake et al. 2018).

A component of the tissue repair capability of CD34+ cells is an anti-inflammatory function. The anti-inflammatory effects of human CD34+ cells have been documented in multiple pre-clinical models including models of severe lung inflammation (Huang et al. 2014; Lo et al. 2017; Abd-Allah et al. 2015). This evidence suggests that the severe pulmonary manifestations of COVID-19 that lead to long term disability and death are mediated by inflammation and vascular damage. CD34+ cells have pre-programmed tissue repair effects mediated by pro-angiogenic and anti-inflammatory functions.

Based on the evidence above, Caladrius has initiated a Phase 1, open-label, proof-of-concept clinical trial that will explore the safety and potential efficacy of peripheral blood derived autologous CD34+ cells (CLBS119) for the repair of COVID-19-induced lung damage in adults. The study will target patients who are experiencing hypoxia due to prior infection with SARS-CoV-2 and who require supplemental oxygen. For more information on this study, please visit



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