Photodynamic therapy (PDT) is an evolving treatment modality that has gained approval from the U.S. Food and Drug Administration for the treatment of various cancers, including microinvasive lung cancer, obstructing esophageal cancer, and non-small cell lung cancer. It is also utilized for premalignant conditions, such as Barrett’s esophagus, and non-oncologic conditions, such as age-related macular degeneration.1 – 4 PDT offers valuable advantages, such as minimal invasion, low systemic toxicity, versatility, and repeatability. However, the optimal clinical outcomes of PDT have been hindered by the lack of a reliable dosimetry metric that accurately quantifies the effective treatment dose, which is essential for predicting and guiding PDT.5 The challenges in achieving accurate dosimetry for PDT stem from its dynamic and complex nature, involving intricate interactions between light, the photosensitizer (PS), and tissue oxygen ().6 In a typical PDT process, the PS is excited by specific wavelengths of treatment light, causing it to transition from its ground state to the excited singlet state. Subsequently, the PS undergoes intersystem crossing, leading to its transition to the triplet state. Type II PDT, the most clinically relevant process, occurs when the triplet state transfers energy to ground-state oxygen, , generating singlet oxygen, . This singlet oxygen induces photodamage in the photosensitized area.7 – 11