Talaporfin (INN, also known as aspartyl chlorin, mono-L-aspartyl chlorin e6, NPe6, or LS11) is a photosensitizer used in photodynamic therapy (PDT). Talaporfin is injected into tumors and other regret tissues where it accumulates. It’s activated with light emitting diodes (LED). It absorbs red light at 664-667 nm normally provided by a laser tuned to this wavelength. It was approved in Japan (in 2004) for PDT of lung cancer and glioma and marketed as Laserphyrin. Clinical and preclinical studies indicate that talaporfin sodium treatment may offer a powerful option to synergize current therapies, as well as an alternative monotherapy in treating cancer.

Porfimer is a photosensitizing agent used in the photodynamic therapy (PDT) of tumors. Porfimer sodium was approved under the brand name PHOTOFRIN for the palliation of patients with completely obstructing esophageal cancer, or of patients with partially obstructing esophageal cancer who, in the opinion of their physician, cannot be satisfactorily treated with Nd:YAG laser therapy. For the reduction of obstruction and palliation of symptoms in patients with completely or partially obstructing endobronchial nonsmall cell lung cancer (NSCLC). For the treatment of microinvasive endobronchial NSCLC in patients for whom surgery and radiotherapy are not indicated. In addition, for the ablation of high-grade dysplasia in Barrett’s esophagus patients who do not undergo esophagectomy. The cytotoxic and antitumor actions of PHOTOFRIN® are light and oxygen dependent. Photodynamic therapy with Porfimer sodium is a two-stage process. The first stage is the intravenous injection of the drug, which mainly is concentrated in the tumor tissues for a longer period. Illumination with 630 nm wavelength laser light constitutes the second stage of therapy. Cellular damage is a consequence of the propagation of radical reactions. Radical initiation may occur after porfimer absorbs light to form a porphyrin excited state. Tumor death also occurs through ischemic necrosis secondary to vascular occlusion that appears to be partly mediated by thromboxane A2 release. The laser treatment induces a photochemical, not a thermal, effect. The necrotic reaction and associated inflammatory responses may evolve over several days.