MaxCyte Regulatory News (MXCT)

MaxCyte, Inc.

("MaxCyte" or the "Company")

MaxCyte Reports Preclinical Results at ASGCT Annual Meeting Showing Correction of Sickle Cell Disease Mutation in Hematopoietic Stem Cells

- Data demonstrate the potential of MaxCyte's technologies in non-viral CRISPR gene correction for the treatment of sickle cell disease

Gaithersburg, Maryland - 21 May 2018: MaxCyte (LSE: MXCT, MXCR), the global cell-based medicines and life sciences company, today announced that preclinical data for its non-viral CRISPR-mediated gene-correction of sickle cell mutation in hematopoietic stem cells (HSC) from a sickle cell disease (SCD) patient were presented at the annual meeting of the American Society of Gene and Cell Therapy (ASGCT) in Chicago on Friday, 18 May 2018.

The new data were presented in a poster presentation, entitled "GMP-compliant non-viral CRISPR-mediated process correcting the sickle cell disease mutation in SCD patient CD34+ cells achieves 60% wild type adult hemoglobin expression in differentiated erythrocytes." The data from work with the National Institutes of Health's (NIH) National Heart Lung and Blood Institute (NHLBI) demonstrated the potential of MaxCyte's technologies and the non-viral CRISPR gene correction in the treatment of SCD.

"We're encouraged that MaxCyte's technology is at the forefront of enabling non-viral CRISPR-mediated correction of disease mutations at clinically-relevant levels," said Doug Doerfler, MaxCyte Chief Executive Officer. "We're excited by these results for their potential to bring therapeutic benefit to individuals living with SCD."

The abstract can be found at the ASGCT meeting website at annualmeetingasgct.com/am18/abstracts and the presentation is available via https://www.maxcyte.com/resource-center/posters-presentations/.

About Sickle Cell Disease

According to the NHLBI, sickle cell disease (SCD) describes a group of inherited red blood cell disorders. Patients with SCD have abnormal hemoglobin, called hemoglobin S or sickle hemoglobin, in their red blood cells. Hemoglobin is a protein in red blood cells that carries oxygen throughout the body. Those who have SCD inherit two abnormal hemoglobin genes, one from each parent. In all forms of SCD, at least one of the two abnormal genes cause a person's body to make hemoglobin S.

Sickle cell disease is a life-long illness. The severity of the disease varies widely from person to person. In high-income countries like the United States, according to NHLBI, the life expectancy of a person with SCD is now about 40-60 years. Currently, hematopoietic stem cell transplantation (HSCT) is the only cure for SCD. Unfortunately, most people with SCD are either too old for a transplant or don't have a relative who is a good enough genetic match for them to act as a donor. A well-matched donor is needed to have the best chance for a successful transplant. While there are some treatments that can reduce symptoms and prolong life, more medical options are needed.

About MaxCyte

MaxCyte is a global cell-based medicines and life sciences company applying its patented cell engineering technology to help patients with high unmet medical needs in a broad range of conditions. MaxCyte is developing novel CARMA therapies for its own pipeline. CARMA is MaxCyte's mRNA-based proprietary platform for autologous cell therapy. In addition, through its core business, the Company leverages its Flow Electroporation® Technology to enable its partners across the biopharmaceutical industry to advance the development of innovative medicines, particularly in cell therapy, including gene editing and immuno-oncology. The Company has placed its cutting-edge flow electroporation instruments worldwide, including with nine of the top ten global biopharmaceutical companies, and has more than 50 partnered programme licences in cell therapy including more than 20 licensed for clinical use. With its robust delivery technology, MaxCyte helps its partners to unlock the full potential of their products.

 For more information, visit www.maxcyte.com.

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