PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
May 29, 2026Journal of Clinical Oncology0 citations

Preclinical investigations and first-in-human phase I trial of KP-483 in solid tumors: Safety, antitumor activity, and preliminary efficacy.

View Full Paper
NYNoboru YamamotoKTKosuke TanakaMSMitsuru Sakuramoto

Key Points

  • This research aims to evaluate the safety and antitumor efficacy of KP-483 in solid tumors.
  • Conducted preclinical studies evaluating KP-483's pharmacodynamic profile and antitumor activity.
  • Enrolled patients in a first-in-human phase I trial with a 3+3 dose-escalation design (jRCT2031220311).
  • Monitored safety, dose-limiting toxicities, and quantified tumor-infiltrating immune cells.
  • KP-483 showed superior EP4 antagonist activity (IC50: 1.0 nmol/L) compared to existing antagonists.
  • In mice, KP-483 led to dose-dependent antitumor effects with increased CD8⁺ T cells and decreased CD163⁺ cells.
  • In 19 patients, KP-483 was well-tolerated with no dose-limiting toxicities, and stable disease was observed in four patients.

Abstract

2659 Background: KP-483 is a novel small-molecule antagonist of the E-type prostanoid receptor 4 (EP4) that potentially exerts antitumor effects by modulating the tumor microenvironment and restoring antitumor immunity. Based on preclinical and phase I studies, this report presents the pharmacological properties, safety, and preliminary efficacy of KP-483. Methods: In preclinical studies, the pharmacodynamic profile of KP-483 was characterized in vitro and in vivo . Antitumor activity was evaluated in tumor-bearing mice, and tumor infiltrating CD8⁺ and CD163⁺ cells were quantified. A first-in-human phase I study (jRCT2031220311) using a 3+3 dose-escalation design enrolled patients with solid tumors who had progressed after standard treatments or for whom no appropriate standard treatment was available. KP-483 was administrated orally once daily, with dose escalation across five cohorts (50, 100, 200, 400, and 800 mg). The primary endpoints were dose-limiting toxicities (DLTs) and safety profiles. Plasma concentrations of KP-483 were also measured. Preliminary efficacy was evaluated according to RECIST criteria, and the antitumor mechanisms were explored by flow cytometry analysis of tumor tissue. Results: KP-483 exhibited greater EP4 antagonist activity than existing antagonists (IC 50 : 1.0 nmol/L in human) and had higher binding affinity to the EP4 receptor and a longer dissociation half-life than PGE 2 in vitro . In mouse models, KP-483 exhibited dose-dependent antitumor effects following 14 days of oral administration at doses of 3, 30, and 300 mg/kg once daily. The number of CD8 + T cells in tumor tissue increased while that of CD163 + cells decreased in a dose-dependent manner. In addition, combination treatment with KP-483 (15 mg/kg, twice daily) and either anti-PD-1 or anti-PD-L1 antibodies enhanced antitumor effects compared with either monotherapy. In the phase I study, safety was assessed in a total of 19 patients. The median treatment duration was 43 days (range: 24–713 days), and no DLTs were observed. The most common treatment-emergent adverse events were anemia and nausea (each 26.3%), with only one study-drug-related grade ≥3 event (anemia). Systemic exposure to KP-483 increased with dose, and the plasma half-life of KP-483 ranged from 7.9 to 12.8 hours on treatment day 15. Best overall responses included stable disease in four patients and partial response in one patient. Flow cytometry analysis of tumor tissue showed a trend toward increased activated cytotoxic T cells, dendritic cells, and M1-like macrophages. Conclusions: KP-483 is a potent EP4 antagonist that exerts antitumor effects through modulation of the tumor immune microenvironment. Given its favorable safety and pharmacokinetic profiles, KP-483 represents a promising EP4 receptor–targeted therapeutic strategy with potential for combination with immune checkpoint inhibitors. Clinical trial information: jRCT2031220311.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Yamamoto et al. (2026) studied this question.

synapsesocial.com/papers/6a192d4afab5b468c44162edhttps://doi.org/10.1200/jco.2026.44.16_suppl.2659
Ask AI
Helpful
Bookmark
Share
View Full Paper