Our selective small-molecule dismutase mimetics are designed to accelerate the conversion of superoxide to hydrogen peroxide, which may be key to reducing radiation treatment-related side effects and increasing the anti-cancer efficacy of these treatments.

The metabolic processing of superoxide is a critical cellular function and part of the broader oxygen metabolic pathways that keep cells functioning. While oxygen metabolic pathways are involved in a host of diseases, Galera is focused on transforming radiation therapy in patients with cancer to both reduce radiation-induced toxicities and improve the anti-cancer efficacy of radiation therapy.



Learn more about our pipeline, including avasopasem manganese (GC4419) and rucosopasem manganese (GC4711).

Superoxide, a highly reactive molecule, is produced by every cell as a part of normal metabolism, but left uncontrolled it is highly toxic, leading to cell damage or cell death. To prevent this, the body produces superoxide dismutase enzymes (SODs), which convert superoxide to hydrogen peroxide. Hydrogen peroxide is much less toxic than superoxide to normal tissue, but more toxic to cancer cells. Radiation therapy induces a large burst of superoxide in the irradiated tissues, which can overwhelm these SODs, damaging normal cells. Such damage to the lining of the mouth, or oral mucosa, is referred to as oral mucositis (OM).

Drugs that mimic native SODs could address the inability of SODs to keep up with the superoxide bursts produced by radiation therapy. The challenge has been finding small molecule dismutase mimetics with similarly fast catalytic rates and high selectivity for superoxide. We have designed, and are developing, our selective dismutase mimetics to have these essential features.

Galera normal cell events

Radiation Therapy-Induced Oral Mucositis

Oral mucositis (OM) is a common and debilitating toxicity for patients being treated with radiation therapy for head and neck cancers (HNC). OM consists of redness (erythema), swelling, sores (ulcers) and breakdown of the oral mucosa, or lining of the oral cavity. OM causes substantial pain and can interfere with the patient’s ability to eat and/or drink.1

Approximately 60-70% of patients with HNC receiving cisplatin and radiation therapy develop Severe Oral Mucositis (SOM) (Grade 3 or Grade 4 OM).


The WHO Scale Criteria for Oral Mucositis1
The WHO Scale Criteria for Oral Mucositis


Radiation therapy-induced OM develops and worsens over time. Patients may experience a sore or burning in their mouth after a week of treatment. Ulceration and more severe, opioid-requiring pain usually develops within the first few weeks of therapy and typically extends over subsequent weeks. OM typically begins to improve 2-4 weeks after the completion of radiation therapy but the final phase of healing may take several months.2

All patients being treated with radiation therapy for head and neck cancer are at risk of experiencing oral mucositis. Oral mucositis can be very painful and can significantly affect nutritional intake, mouth care, and quality of life.3

There is currently no FDA-approved drug therapy approved to reduce or prevent the incidence or duration of SOM in head and neck cancer or any solid tumors.

Until more research is available, pain relief, dietary support, and secondary infection prevention are key elements for management of oral mucositis.5



Harnessing the Anticancer Power of Hydrogen Peroxide

As cancer cells are more susceptible than normal cells to increased levels of hydrogen peroxide, we believe the conversion of radiation-generated superoxide to hydrogen peroxide by our selective dismutase mimetics can improve outcomes for patients who receive radiation therapy.

cancer cell events

In preclinical models of pancreatic ductal adenocarcinoma (PDAC) and non-small cell lung cancer (NSCLC) and other cancers, our selective dismutase mimetics increased anticancer activity of high daily doses of radiation therapy similar to those used in Stereotactic Body Radiation Therapy (SBRT) for patients with cancer.6

panc 1 pdac xenografts

H1299 NSCLC Xenografts
H1299 NSCLC Xenografts
H1299 NSCLC Xenografts
H1299 NSCLC Xenografts
H1299 NSCLC Xenografts


Activity of high fraction dose radiation therapy is significantly enhanced by selective dismutase mimetics in cancer preclinical models.


Preclinical studies of mechanism show that our selective dismutase mimetics synergize with SBRT by generating hydrogen peroxide. For example, when tumors are genetically engineered to make catalase, which removes hydrogen peroxide, the boost in SBRT efficacy is no longer seen.6

h12299 cat nsclc mouse model


Aiming to Transform Outcomes for Patients With Locally Advanced Pancreatic Cancer

Pancreatic cancer incidence is rising, and this tumor is expected to become the second leading cause of cancer-related death in the United States by 2030.7 Over 60,000 people in the United States are estimated to be diagnosed with pancreatic cancer in 2022. The 5-year survival rate for all stages combined is only 11%. For the small percentage (13%) of patients diagnosed with local disease, the 5-year survival rate is 42%.8 Novel therapies to improve survival for patients with pancreatic cancer are needed.

Stereotactic body radiation therapy (SBRT) is increasingly used for locally advanced pancreatic cancer.9 SBRT is typically given in 3 to 5 large fractions.10  Even with the use of SBRT, the opportunity for improvement in treatment outcomes is substantial.

In a pilot Phase 1/2 trial, patients with locally advanced pancreatic cancer were randomized to receive SBRT plus either placebo or a rucosopasem analogue. This trial appears to demonstrate acceptable safety in combination with SBRT (10-11 Gy x 5), as well as suggesting improvements in overall survival, progression-free survival, locoregional control, and time to distant metastases. These data support the hypothesis currently being tested in the GRECO-2 trial that rucosopasem may improve overall survival in combination with SBRT compared to SBRT alone.11

Group Chart - Slide 1 - OS / PFS / Locoregional Control / Distant Metastases Control
Group Chart - Slide 2 - showing line for Placebo + RT in all 4 charts
Group Chart - Slide 3 - showing line for DM + RT in all 4 charts

Click to enlarge.

Minimum 12-month follow-up on all patients. DMC and LRC defined as distant metastasis or local regional progression, not censored for treatment post SBRT.

Rucosopasem combined with SBRT is being studied as it may improve survival in patients with locally advanced pancreatic cancer.



  1. World Health Organization. (1979). WHO handbook for reporting results of cancer treatment. World Health Organization.
  2. Wong PC, Dodd MJ, Miaskowski C, et al. Mucositis pain induced by radiation therapy: prevalence, severity, and use of self-care behaviors. J Pain Symptom Manag 2006;32:27-37.
  3. Lalla R, Sonis S, Peterson D. Management of oral mucositis in patients who have cancer. Dent Clin North Am. 2008; 52: 61–77.
  4. Galera Market Research. Data on File. 2021
  5. Elad S, Cheng KKF, Lalla RV, et al. MASCC/ISOO clinical practice guidelines for the management of mucositis secondary to cancer therapy. Cancer. 2020;126:4423-4431.
  6. Sishc BJ, et al. Avasopasem manganese synergizes with hypofractionated radiation to ablate tumors through the generation of hydrogen peroxide. Sci Transl Med. 2021;13:eabb3768.
  7. Rahib L, et al. Projecting cancer incidence and deaths to 2030: The unexpected burden of thyroid, liver, and pancreas cancers in the United States. Clin Cancer Res. 2014;74:2913-2921.
  8. American Cancer Society. Cancer Facts & Figures 2022. Available at:
  9. Ghaly M, Gogineni E, Herman J, Saif MW. New potential options for SBRT in pancreatic cancer. Cancer Med J. 2021 March;4(Suppl 3): 41–50.
  10. Galera Therapeutics, Inc. Galera announces final results from pancreatic cancer trial showing improvements on all efficacy parameters. Press Release. September 8, 2021. Accessed December 21, 2021.


Investigational Drugs – Not for Commercial Distribution