Aprea Therapeutics is dedicated to advancing precision medicine in oncology, focusing on delivering targeted therapies that align with specific cancer-associated genetic mutations. The company employs a strategy centered on synthetic lethality, which involves developing small molecule inhibitors that selectively target cancer cells while sparing normal tissues. This innovative approach aims to enhance the therapeutic window, thereby increasing the effectiveness of treatments and minimizing adverse effects. By matching therapies to the genetic profile of tumors, Aprea seeks to improve patient outcomes and reduce the likelihood of treatment resistance.

The company’s pipeline is robust, exploring multiple therapeutic targets to maximize the potential for successful treatment outcomes. Aprea is actively engaged in clinical trials to bring its DDR-targeted therapies to market, reflecting its commitment to pioneering advancements in cancer treatment. Through its unique focus on DDR (DNA Damage Response) mechanisms, Aprea Therapeutics is positioned to revolutionize cancer care by providing solutions that are tailored to the genetic makeup of individual tumors, ultimately aiming to save lives through innovative therapeutic strategies.

United States

Aprea Therapeutics Inc., (NASDAQ: APRE) is a biopharmaceutical company headquartered in Boston, Massachusetts with research facilities in Stockholm, Sweden, focused on developing and commercializing novel cancer therapeutics to reactivate the mutant tumor suppressor protein p53, the most commonly mutated gene in cancer

Cancer

Aprea Therapeutics

Solid tumor/s

ATRN-119 is a potent and highly selective first-in-class macrocyclic ATR inhibitor, designed to be used in patients with mutations in DDR-related genes. Cancers with mutations in DDR-related genes represent a high unmet medical need. Patients with DDR-related gene mutations have a poor prognosis and, currently, have no effective therapies.

ATRN-119

APR-1051 is a potent and selective small molecule that has been designed to potentially solve liabilities and may achieve greater clinical activity than other WEE1 programs currently in development. Aprea is advancing APR-1051 as monotherapy in cancers with Cyclin E over expression, as well as other biomarkers that are predicted to be sensitive to WEE1 inhibition. Cancers overexpressing Cyclin E represent a high unmet medical need. Patients with Cyclin E overexpression have poor prognosis and, currently, have no effective therapies.

APR-1051

Small Molecule Pharmaceuticals

Blood disorder

Myelodysplastic syndrome

Eprenetapopt (APR-246) is a small molecule that has demonstrated reactivation of mutant and inactivated p53 protein – by restoring wild-type p53 conformation and function – thereby inducing programmed cell death in human cancer cells. Pre-clinical anti-tumor activity has been observed with eprenetapopt in a wide variety of solid and hematological cancers, 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 1/2 clinical program with eprenetapopt 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.

Eprenetapopt (APR-246)  + Azacitidine

Acute myeloid leukemia

When APR-246 is administered to patients it is converted into the active drug, methylene quinuclidinone (MQ). MQ binds to p53 at two cysteine residues in the DNA-binding domain and stabilizes mutant p53 in the normal, functional structure. Research conducted by our founders and our collaborators have confirmed not only the sites where MQ binds to mutant p53 but also the restoration of the correct protein structure. Stabilization of normal protein structure – the key step in the APR-246 mechanism of action – reactivates mutant p53, which can then trigger responses such as cell cycle arrest and apoptosis.
MQ not only restores the ability of a cell to response to oxidative stress and DNA damage via reactivation of mutant p53 but also produces severe and sustained oxidative stress to which reactivated p53 can respond. The overlap of these features, linked together by MQ, may in turn provide more efficient induction of apoptosis and elimination of cancer cells.

Eprenetapopt (APR-246) + azacitidine 

Mutant Myelodysplastic Syndromes

APR-548, is a next-generation p53 reactivator that is being developed in an oral dosage form.

APR-548 + azacitidine 

Boston, Massachusetts, United States of America

Aprea Therapeutics

Company Details