BOSTON and STOCKHOLM, Feb. 27, 2019 /PRNewswire/ -- Aprea Therapeutics, a clinical-stage biotechnology company developing novel anticancer therapies targeting the p53 tumor suppressor protein, today announced that funds managed by Janus Henderson Investors joined its Series C financing as a new investor, raising the total amount of the financing to EUR 55 million. Janus Henderson Investors joins the financing round closed in November, 2018 and led by Redmile Group, with participation by Rock Springs Capital and existing investors: 5AM Ventures, Versant Ventures, HealthCap, Sectoral Asset Management and Karolinska Development AB (Nasdaq Stockholm: KDEV).
"The addition of Janus to our investor group further broadens our US investor base and better positions the company to both advance its clinical strategy in hematological malignancies and take advantage of future strategic opportunities," said Christian S. Schade, President and Chief Executive Officer of Aprea Therapeutics.
Proceeds from the financing will be used to advance the clinical development of APR-246, a first-in-class anticancer agent that reactivates mutated p53 tumor suppressor protein. Aprea has commenced a Phase 3 clinical study in myelodysplastic syndromes (MDS) and has completed enrollment in a Phase Ib/II clinical trial in p53 mutated high-risk myelodysplastic syndromes (MDS) and oligoblastic acute myeloid leukemia (AML) with APR-246 and azacitidine. Additional studies in MDS and AML are underway and in planning with other approved agents.
About Myelodysplastic Syndromes
Myelodysplastic syndromes (MDS) represents a spectrum of hematopoietic stem cell malignancies in which bone marrow fails to produce sufficient numbers of healthy blood cells. Approximately 30-40% of MDS patients progress to acute myeloid leukemia (AML) and mutation of the p53 tumor suppressor protein is thought to contribute to disease progression. Mutations in p53 are found in up to 20% of MDS and AML patients and are associated with poor overall prognosis.
About p53 and APR-246
The p53 tumor suppressor gene is the most frequently mutated gene in human cancer, occurring in approximately 50% of all human tumors. These mutations are often associated with resistance to anti-cancer drugs and poor overall survival, representing a major unmet medical need in the treatment of cancer.
APR-246 has been shown to reactivate mutant and inactivated p53 protein – by restoring wild-type p53 conformation and function – and thereby induce programmed cell death in human cancer cells. APR-246 has demonstrated pre-clinical anti-tumor activity in a wide variety of solid and hematological (blood) tumors, including MDS, AML, and ovarian cancer, among others. Additionally, strong synergy has been seen with both traditional anti-cancer agents, such as chemotherapy, as well as newer mechanism-based anti-cancer drugs and immuno-oncology checkpoint inhibitors. In addition to pre-clinical testing, a Phase I/II clinical program with APR-246 has been completed, demonstrating a favorable safety profile and both biological and confirmed clinical responses in hematological malignancies and solid tumors with mutations in the TP53 gene.
About Aprea Therapeutics
Aprea Therapeutics is a Boston, Massachusetts- and Stockholm, Sweden-based biopharmaceutical company focused on the discovery and development of novel anticancer compounds that reactivate the tumor suppressor protein, p53. The Company's lead drug candidate is APR-246, a first-in-class small molecule, is in clinical development for myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), as well as additional hematologic and solid tumor malignancies. Aprea is also developing second generation p53 reactivators that have best-in-class potential. For more information, please visit www.apreatherapeutics.com.
Corporate Contacts:
Christian S. Schade
President and Chief Executive Officer
Gregory A. Korbel
Vice President of Business Development
SOURCE Aprea Therapeutics AB
Related Links
http://www.apreatherapeutics.com
WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM?
Newsrooms &
Influencers
Digital Media
Outlets
Journalists
Opted In
Share this article