[Asia Economy Reporter Hyunseok Yoo] Pamfexin, a company specializing in antibody drug development, announced on the 10th that it has confirmed the possibility of treating macular degeneration through a vascular normalization mechanism rather than the conventional neovascular blocking method.
On the 5th, Pamfexin presented the non-clinical results of its next-generation vascular disease treatment candidate PMC-403 at the annual meeting of the Association for Research in Vision and Ophthalmology (ARVO), held online in the United States.
‘PMC-403,’ under development by Pamfexin, is a first-in-class innovative drug candidate that restores abnormally developed neovascular vessels to normal vascular forms. The target indication of PMC-403, wet macular degeneration, is an age-related blindness disease that progresses rapidly and causes severe vision loss.
Due to the global aging trend, the market size is expected to reach 20 trillion KRW by 2028. However, all currently used treatments for macular degeneration are anti-VEGF (vascular endothelial growth factor) drugs. These have limitations such as low response rates, resistance, and poor patient compliance due to frequent dosing, resulting in high unmet medical needs.
Unlike existing treatments, PMC-403 is differentiated by its vascular normalization mechanism, making it applicable even to patients who do not respond to anti-VEGF agents.
The company stated that in the recent ARVO presentation, PMC-403 showed a blood leakage suppression effect comparable to that of ‘Aflibercept,’ a blockbuster drug and macular degeneration treatment. Specifically, the Tie2 activation marker p-Tie2 increased in a concentration-dependent manner with PMC-403, confirming its Tie2 activation mechanism. Additionally, in laser-induced choroidal neovascularization (CNV) efficacy evaluation models in mice and primates, which mimic wet macular degeneration, PMC-403 demonstrated blood leakage suppression efficacy comparable to existing treatments.
Furthermore, after administration, levels of angiogenic factors ANG2 and VEGF, which are secreted during blood leakage, were significantly reduced, confirming the efficacy of PMC-403 in reducing neovascularization factors indirectly alongside its vascular normalization mechanism.
Yujin San, CEO of Pamfexin, said, "The non-clinical results of PMC-403 announced this time are meaningful in that they secured results showing that the existing neovascular inhibition effect can also be achieved through a vascular normalization mechanism." He added, "We expect this to overcome the limitations of existing treatments that block neovascular formation." He further stated, "We aim to validate PMC-403’s potential at a global conference involving ophthalmologists and researchers worldwide, conduct toxicity tests necessary for submitting the Investigational New Drug (IND) application, and start clinical trials next year."
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