Temporin-Sha is an antimicrobial peptide known for its broad-spectrum biological activity. It is effective against Gram-positive bacteria (such as Listeria, MIC= 6.25 μM), Gram-negative bacteria (such as Escherichia coli, MIC= 10 μM), and resistant strains like Methicillin-resistant Staphylococcus aureus. Additionally, Temporin-Sha inhibits Candida albicans (MIC= 25 μM), Saccharomyces cerevisiae (MIC= 12 μM), Leishmania promastigotes and amastigotes (IC50= 9-20 μM), and Trypanosomes (IC50= 17 μM). It also exhibits antiviral activity against HSV-1 and shows anticancer properties, displaying cytotoxicity towards breast cancer cells MCF-7 and lung cancer cells H460.

Temporin-Sha, at a concentration of 12.5 μM for 3 hours, leads to membrane rupture of Listeria ivanovii and maintains over 75% bactericidal efficiency even when grafted onto a gold surface. It exhibits notable inhibitory effects on both Fluconazole-sensitive (CaS) and Fluconazole-resistant (CaR) strains of Candida albicans (MIC ≥ 256 μg/mL), suppressing biofilm formation and disrupting preformed biofilms at high concentrations (1024 μg/mL). Across all concentrations (32-1024 μg/mL), Temporin-Sha shows no cytotoxicity to normal oral keratinocytes (NOK-si) (CC50 = 3805 μg/mL) and exhibits mild cytotoxicity to human gingival fibroblasts (FGH) (CC50 = 492 μg/mL). In human primary keratinocytes, Temporin-Sha (1.25-10 μM, 25 h) significantly inhibits HSV-1 DNA replication by directly disrupting viral particles, independent of immune modulation. It effectively alters membrane integrity in bacteria (Escherichia coli, Streptococcus pyogenes, Klebsiella pneumoniae, Lactobacillus) and parasites (T. cruzi), inducing apoptosis-like death in Leishmania infantum promastigotes. Temporin-Sha, after 55 generations of E. coli continuous culture up to 60 days, shows no tendency to promote bacterial resistance, unlike Ampicillin. Additionally, it demonstrates cytotoxicity against various cancer cell lines, with IC50 values of 14.47 μM (MCF-7), 18.36 μM (HeLa), and 34.5 μM (NCI-H460), primarily inducing necrosis rather than apoptosis.