Key Takeaways
- •Bocharov, A. V., et al. (2016). Synthetic amphipathic helical peptides targeting CD36 attenuate lipopolysaccharide-induced inflammation and acute lung injury. *The Journal of Immunology*, 197(2), 611-619.
- •Casu, C., et al. (2016). Minihepcidin peptides as disease modifiers in mice affected by β-thalassemia and polycythemia vera. *Blood*, 128(2), 265-276.
- •Teng, Y., et al. (2016). Targeting the WASF3-CYFIP1 complex using stapled peptides suppresses cancer cell invasion. *Cancer Research*, 76(4), 965-973.
- •Vaudry, H., et al. (2015). International Union of Basic and Clinical Pharmacology. XCII. Urotensin II, Urotensin II-Related Peptide, and Their Receptor: From Structure to Function. *Pharmacological Reviews*, 67(1), 214-258.
Synthetic Helical Peptides Combat Acute Lung Injury
Synthetic amphipathic helical peptides, designed to mimic apolipoprotein A-I, bind to class B scavenger receptors including SR-BI, SR-BII, and CD36. These receptors handle lipid transport and pathogen detection. One study tested such peptides for their capacity to lessen LPS-triggered inflammation, endothelial barrier issues, and acute lung injury.
L37pA, which equally targets CD36 and SR-BI, blocked LPS-induced IL-8 release and barrier problems in endothelial cell cultures. It also cut lung neutrophil influx by 40% in mice with LPS-induced acute lung injury. Testing 20 such peptides in HEK293 cells engineered with different scavenger receptors pinpointed those favoring CD36.
Among peptides hitting SR-BI/BII and CD36, ELK-B mainly used CD36. ELK-B outperformed L37pA, 5A, and ELK in curbing LPS-caused pulmonary barrier failure, neutrophil entry to lungs, and lung swelling. Peptides selective for CD36 prove stronger against acute lung inflammation and impairment, suggesting CD36-focused strategies as treatments for inflammation-driven acute lung injury and pulmonary edema.
Minihepcidins Address β-Thalassemia and Polycythemia Vera
Disrupted red blood cell production causes major issues in β-thalassemia and polycythemia vera. β-Thalassemia features faulty erythropoiesis, low red blood cell output, anemia, and excess iron, while polycythemia vera involves too many red blood cells and clot risks. Minihepcidins, as hepcidin activators, previously curbed iron buildup in hemochromatosis mouse models and limited erythropoiesis with higher doses via iron restriction.
These minihepcidin peptides present a promising option for controlled iron restriction in β-thalassemia, polycythemia vera, and similar erythropoiesis disorders. For detailed peptide properties, consult the Peptide Glossary.
Stapled Peptides Block Cancer Cell Invasion
Cancer cells constantly produce WASF3, a protein silent in healthy cells, aiding tumor spread. WASF3 supports invasion and maintains stability by linking to CYFIP1. Researchers first noted WASF3's metastasis role in 2002 from a neuroblastoma case, then confirmed by gene knockout halting spread.
Mass spectrometry revealed CYFIP1 as a top WASF3 partner. Stapled peptides now sever this WASF3-CYFIP1 bond. One clinical trial already tests a peptide disrupting another protein pair, signaling growing interest in such approaches.
Humanin Derivatives Protect Against Necrosis in Strokes and Injuries
Strokes, heart attacks, and traumatic brain injuries share oxygen deprivation leading to cell death. Oxygen lack triggers signals that stop ATP production. Derivatives of humanin, a mitochondrial-encoded peptide, aim to halt this, preserving tissue viability.
These humanin analogs counteract ATP drops from necrosis. AGA(C8R)-HNG17 and AGA-HNG protected neuronal cells when given before a necrotic agent. Such compounds offer leads for necrosis-linked disease therapies. Use tools like the Half-Life Calculator for peptide stability in research.
FKBPL-Mimicking Peptide Gains FDA Orphan Status for Ovarian Cancer
A novel therapeutic peptide copies traits of FKBPL, a natural protein affecting tumor processes like stem cells and blood vessel growth. Initial work by Professor Tracy Robson laid the foundation. The U.S. Food and Drug Administration recently awarded Orphan Drug Designation to this candidate for ovarian cancer treatment.
Urotensin II Influences Multiple Systems
Urotensin II, a cyclic neuropeptide, was first found in teleost fish urophysis for its hindgut contraction effect. It signals via the UT G protein-coupled receptor, altering paths like intracellular calcium. UII constricts some vessels but widens others, impacting heart, kidneys, and brain functions.
Key Studies and Takeaways
These findings from 2015-2016 studies underscore peptides' versatility against inflammation, blood disorders, cancer, necrosis, and more:
- Bocharov, A. V., et al. (2016). Synthetic amphipathic helical peptides targeting CD36 attenuate lipopolysaccharide-induced inflammation and acute lung injury. The Journal of Immunology, 197(2), 611-619.
- Casu, C., et al. (2016). Minihepcidin peptides as disease modifiers in mice affected by β-thalassemia and polycythemia vera. Blood, 128(2), 265-276.
- Teng, Y., et al. (2016). Targeting the WASF3-CYFIP1 complex using stapled peptides suppresses cancer cell invasion. Cancer Research, 76(4), 965-973.
- Vaudry, H., et al. (2015). International Union of Basic and Clinical Pharmacology. XCII. Urotensin II, Urotensin II-Related Peptide, and Their Receptor: From Structure to Function. Pharmacological Reviews, 67(1), 214-258.
Peptide research continues to reveal targeted therapies for complex diseases. Explore our Free peptide tools for study support.