ArticlePeptides2015
ML-18 is a non-peptide bombesin receptor subtype-3 antagonist which inhibits lung cancer growth.
Article in Peptides, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Identification of a Novel Antagonist of BRS-3 from Natural Products and Its Protective Effects Against HInternational journal of molecular sciences · 2025Article
- Bombesin Receptor Subtype-3 Regulates Tumor Growth by HER2 Tyrosine Phosphorylation in a Reactive Oxygen Species-Dependent Manner in Lung Cancer Cells.Targets (Basel) · 2025Article
- Bombesin-like receptor 3 expression induced by bisphenol A is likely associated with reduced cell proliferation by inhibiting DNA synthesis and inducing inflammation in liver cells.Molecular biology reports · 2024Article
- GPCR-mediated EGFR transactivation ameliorates skin toxicities induced by afatinib.Acta pharmacologica Sinica · 2022Article
- Identification and Validation of Immune Cells and Hub Genes in Gastric Cancer Microenvironment.Disease markers · 2022Article
- New Insights into the Stereochemical Requirements of the Bombesin BB1 Receptor Antagonists Binding.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Preclinical Evaluation of NHS-Activated Gold Nanoparticles Functionalized with Bombesin or Neurotensin-Like Peptides for Targeting Colon and Prostate Tumours.Molecules (Basel, Switzerland) · 2020Article
- Peptide receptors as cancer drug targets.Annals of the New York Academy of Sciences · 2019Review
- Development and Characterization of a Novel, High-Affinity, Specific, Radiolabeled Ligand for BRS-3 Receptors.The Journal of pharmacology and experimental therapeutics · 2019Article
- A possible new target in lung-cancer cells: The orphan receptor, bombesin receptor subtype-3.Peptides · 2018Article
- Exploiting cancer's phenotypic guise against itself: targeting ectopically expressed peptide G-protein coupled receptors for lung cancer therapy.Oncotarget · 2017Review
- AM-37 and ST-36 Are Small Molecule Bombesin Receptor Antagonists.Frontiers in endocrinology · 2017Article
- Molecular basis for high affinity and selectivity of peptide antagonist, Bantag-1, for the orphan BB3 receptor.Biochemical pharmacology · 2016Article
- Transactivation of Epidermal Growth Factor Receptor by G Protein-Coupled Receptors: Recent Progress, Challenges and Future Research.International journal of molecular sciences · 2016Review
- Review
- Bombesin receptor subtype 3 as a potential target for obesity and diabetes.Expert opinion on therapeutic targets · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Bombesin receptor subtype (BRS)-3 is a G protein coupled receptor (GPCR) for the bombesin (BB)-family of peptides. BRS-3 is an orphan GPCR and little is known of its physiological role due to the lack of specific agonists and antagonists. PD168368 is a nonpeptide antagonist for the neuromedin B (NMB) receptor (R) whereas PD176252 is a nonpeptide antagonist for the gastrin releasing peptide (GRP) R and NMBR but not BRS-3. Here nonpeptide analogs of PD176252 e.g. the S-enantiomer ML-18, and the R-enantiomer, EMY-98, were investigated as BRS-3 antagonists using lung cancer cells. ML-18 and EMY-98 inhibited specific (125)I-BA1 (DTyr-Gln-Trp-Ala-Val-βAla-His-Phe-Nle-NH2)BB(6-14) binding to NCI-H1299 lung cancer cells stably transfected with BRS-3 with IC50 values of 4.8 and >100μM, respectively. In contrast, ML-18 bound with lower affinity to the GRPR and NMBR with IC50 values of 16 and >100μM, respectively. ML-18 (16μM), but not its enantiomer EMY-98, inhibited the ability of 10nM BA1 to elevate cytosolic Ca(2+) in a reversible manner using lung cancer cells loaded with FURA2-AM. ML-18 (16μM), but not EMY-98, inhibited the ability of 100nM BA1 to cause tyrosine phosphorylation of the EGFR and ERK in lung cancer cells. ML-18 but not EMY-98 inhibited the proliferation of lung cancer cells. The results indicate that ML-18 is a nonpeptide BRS-3 antagonist that should serve as a template to improve potency and selectivity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.