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Preclinical data indicate modulation of inflammatory and pro-fibrotic signalling pathways relevant to lung fibrosis, yet direct demonstration of reduced fibroblast activation or collagen deposition in established pulmonary fibrosis models is currently lacking

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No, but they are closely related

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In smoking-associated chronic inflammatory environments, the upregulation of PTPRS and SFRP2 on fibroblasts aligns with previous studies demonstrating increased expression of these markers in fibroblasts with a pro-inflammatory phenotype

MT2 is the more powerful, broader-acting compound, which also makes precise dosing an absolutely critical, non-negotiable element of any study