ArticleInternational journal of molecular sciences2022
Enhanced Therapeutic Effect of Optimized Melittin-dKLA, a Peptide Agent Targeting M2-like Tumor-Associated Macrophages in Triple-Negative Breast Cancer.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Melittin, A Potential Game-changer in the Fight Against Breast Cancer: A Systematic Review.Anti-cancer agents in medicinal chemistry · 2025Pooled it
- Venom-Derived Peptides in Breast Cancer: Pharmacological Mechanisms and Medicinal Chemistry-Guided Translational Development.Archiv der Pharmazie · 2026Review
- Multidimensional Modification and Functional Optimization of Melittin: From Natural Toxic Peptide to Safe and Effective Therapeutics.Pharmaceutics · 2026Review
- Peptide-mediated immunomodulation of tumor microenvironment in triple-negative breast cancer: A comprehensive review.The Journal of pharmacology and experimental therapeutics · 2026Review
- CD18-targeted peptide-drug conjugate remodels the immunosuppressive tumor microenvironment of prostate cancer by selective depletion of M2 macrophages.NPJ precision oncology · 2026Article
- Targeted biologics for TNBC: Advances in nanobodies, antibodies, peptides, and aptamers.Molecular therapy. Oncology · 2026Review
- Therapeutic Bioactivity Exerted by theMolecules (Basel, Switzerland) · 2025Article
- Melittin-Based Nanoparticles for Cancer Therapy: Mechanisms, Applications, and Future Perspectives.Pharmaceutics · 2025Review
- The Combination of CD300c Antibody with PD-1 Blockade Suppresses Tumor Growth and Metastasis by Remodeling the Tumor Microenvironment in Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Article
- Myristoyl-CM4 Exhibits Direct Anticancer Activity and Immune Modulation in Hepatocellular Carcinoma: Evidence from In Vitro and Mouse Model Studies.International journal of molecular sciences · 2025Article
- Conformation-sensitive targeting of CD18 depletes M2-like tumor-associated macrophages resulting in inhibition of solid tumor progression.Journal for immunotherapy of cancer · 2025Article
- Applying integrated transcriptome and single-cell sequencing analysis to develop a prognostic signature based on M2-like tumor-associated macrophages for breast cancer.Discover oncology · 2025Article
- Dynamic Visualization of Computer-Aided Peptide Design for Cancer Therapeutics.Drug design, development and therapy · 2025Review
- The current landscape of the antimicrobial peptide melittin and its therapeutic potential.Frontiers in immunology · 2024Review
- Melittin: a possible regulator of cancer proliferation in preclinical cell culture and animal models.Journal of cancer research and clinical oncology · 2023Review
- Facts and prospects of peptide in targeted therapy and immune regulation against triple-negative breast cancer.Frontiers in immunology · 2023Review
- Tumor-associated macrophages in nanomaterial-based anti-tumor therapy: as target spots or delivery platforms.Frontiers in bioengineering and biotechnology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is characterized by a high possibility of metastasis. M2-like tumor-associated macrophages (TAMs) are the main components of the tumor microenvironment (TME) and play a key role in TNBC metastasis. Therefore, TAMs may be a potential target for reducing TNBC metastasis. Melittin-dKLA, a peptide composed of fused melittin and pro-apoptotic peptide d(KLAKLAK)2 (dKLA), showed a potent therapeutic effect against cancers by depleting TAMs. However, melittin has a strong adverse hemolytic effect. Hence, we attempted to improve the therapeutic potential of melittin-dKLA by reducing toxicity and increasing stability. Nine truncated melittin fragments were synthesized and examined. Of the nine peptides, the melittin-dKLA8-26 showed the best binding properties to M2 macrophages and discriminated M0/M1/M2. All fragments, except melittin, lost their hemolytic effects. To increase the stability of the peptide, melittin-dKLA8-26 fragment was conjugated with PEGylation at the amino terminus and was named PEG-melittin-dKLA8-26. This final drug candidate was assessed in vivo in a murine TNBC model and showed superior effects on tumor growth, survival rates, and lung metastasis compared with the previously used melittin-dKLA. Taken together, our study showed that the novel PEG-melittin-dKLA8-26 possesses potential as a new drug for treating TNBC and TNBC-mediated metastasis by targeting TAMs.
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Registered trials
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