ReviewReported positiveLimited evidenceTier 4 · clinical
Drugs · Jun 2026 · regulatory approval summary
Relacorilantepithelial ovarian cancerfallopian tube cancerprimary peritoneal cancerpancreatic cancerprostate cancer Relacorilant is a non-steroidal, selective glucocorticoid receptor antagonist being developed for several solid tumours and Cushing syndrome. The article reports that relacorilant received its first approval in the USA on 25 March 2026 for use in combination with nab-paclitaxel for adults with platinum-resistant epithelial ovarian, fallopian tube or primary peritoneal cancer after 1-3 prior systemic regimens (at least one including bevacizumab). The article summarizes development milestones leading to this approval.
Studied with: nab-paclitaxel.
Key findings
- Relacorilant is a non-steroidal, selective glucocorticoid receptor II antagonist developed by Corcept Therapeutics.
- Relacorilant received first approval in the USA on 25 March 2026.
- Approval is for use in combination with nab-paclitaxel for adults with platinum-resistant epithelial ovarian, fallopian tube or primary peritoneal cancer who have received 1-3 prior systemic treatment regimens, at least one of which included bevacizumab.
- Relacorilant is being developed for various solid tumours including ovarian, fallopian tube, peritoneal, pancreatic and prostate cancers, as well as for Cushing syndrome.
- The article summarizes milestones in the development of relacorilant leading to this approval.
Limitations: Abstract provides no efficacy or safety outcome data or numeric results from trials.; No trial design, sample size, or methods are reported in the abstract.; This is an approval/summary article, not primary trial data.; Geographic scope limited to a USA approval; supporting evidence is not detailed in the abstract..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Animal studyReported positivePreclinical onlyTier 2 · animal
Science (New York, N.Y.) · Mar 2026
pancreatic cancer
The authors report that drugs which inhibit KRAS signaling delayed the development of pancreatic cancer in mice. The abstract does not specify which drugs, doses, timing, sample size, or statistical measures were used. This is an animal study showing a preclinical anticancer effect of KRAS-pathway inhibition.
Key findings
- In mice, drugs that inhibit KRAS signaling delayed the development of pancreatic cancer.
Limitations: Study was performed in mice (animal model) and results may not translate to humans.; Abstract provides no details on which specific drugs were used, doses, timing, sample sizes, control groups, or statistical significance.; No quantitative results or methodology are reported in the abstract..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
OtherMechanismReported negativePreclinical onlyTier 1 · lab
Cell metabolism · Dec 2025
pancreatic cancer
This study examined mechanisms linking obesity to pancreatic cancer progression. It reports that extracellular vesicles from visceral adipose tissue reprogram immune cells via a cathepsin A–pseudouridine–mast cell axis. The authors conclude this pathway promotes immune evasion and resistance to checkpoint blockade therapy in pancreatic cancer.
Key findings
- Extracellular vesicles from visceral adipose tissue reprogram immune cells.
- This reprogramming occurs through a cathepsin A–pseudouridine–mast cell axis.
- The described mechanism provides a way obesity can drive immune evasion and resistance to checkpoint blockade therapy in pancreatic cancer.
Limitations: Abstract does not state the experimental model(s) used (cells, animals, or human tissue) or sample sizes.; No quantitative data, statistical results, or numeric effect sizes are reported in the abstract.; Abstract provides mechanistic insight but does not present clinical trial or patient outcome data to demonstrate relevance in humans..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewInconclusiveLimited evidenceTier 4 · clinical
World journal of gastroenterology · Nov 2025 · narrative review
pancreatic neoplasmspancreatic cancer
This is a narrative review summarizing recent progress in pancreatic cancer up to 2025. The authors discuss advances in prevention and early detection, better molecular understanding, more effective systemic therapies, improved quality of life and surgical outcomes, and the role of artificial intelligence.
Key findings
- Pancreatic cancer continues to have a very poor prognosis due to late presentation, aggressive biology, and resistance to chemotherapy.
- Areas of progress highlighted include prevention and early detection strategies.
- The review notes refinements in molecular understanding of pancreatic cancer that may inform therapy.
- Identifying more effective systemic therapies and improving quality of life and surgical outcomes are described as progress areas.
- The authors emphasize the importance of technological advances, particularly artificial intelligence.
Limitations: Narrative review; no original experimental or clinical data are reported in the abstract.; Abstract provides no methods, selection criteria, or systematic search details.; No quantitative results or specific studies/metrics are reported in the abstract.; Broad scope limits detail on any single intervention, biomarker, or therapy..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Animal studyFormulationReported positivePreclinical onlyTier 2 · animal
Journal of nanobiotechnology · Jul 2025
pancreatic cancer
The authors developed a PLGA/polydopamine nanoparticle carrying manganese porphyrin and the hypoxia-activated prodrug tirapazamine, labeled with 131I for dual MRI/SPECT imaging. In preclinical experiments the platform generated ROS under ultrasound combined with 131I beta emissions, exacerbated tumor hypoxia to activate TPZ, and produced synergistic tumor-cell killing while inhibiting tumor stem cell formation. The nanoparticle showed good biocompatibility, stable radionuclide labeling, and enabled real-time imaging of its metabolism and therapeutic effect.
Studied with: 131I radionuclide therapy, sonodynamic therapy (ultrasound).
Key findings
- MnTTP and tirapazamine (TPZ) were encapsulated in PLGA spheres and coated with polydopamine to allow labeling with 131I, creating a theranostic nanoplatform.
- The nanoplatform demonstrated excellent biocompatibility, stable labeling efficiency, and dual-modal MRI/SPECT imaging capabilities.
- Under ultrasound activation the nanoplatform generated ROS, and in combination with beta-rays emitted by 131I synergistically eradicated tumor cells and exacerbated tumor hypoxia.
- TPZ was activated under hypoxic conditions to produce toxic free radicals, enabling synergistic radionuclide and sonodynamic therapy.
- The combined approach effectively inhibited tumor stem cell formation and enhanced anti-tumor efficacy, with in vivo metabolism and therapeutic effect monitored by MRI/SPECT.
Limitations: Preclinical study reported in the abstract (in vivo models) with no human data.; Abstract does not report species, sample sizes, or quantitative effect sizes.; No details on controls, comparator groups, or statistical significance are provided in the abstract.; Safety, long-term outcomes, and translatability to humans are not addressed in the abstract..
Preclinical study of a theranostic nanoparticle combining radionuclide and sonodynamic approaches with a hypoxia-activated prodrug for pancreatic cancer.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewInconclusiveLimited evidenceTier 4 · clinical
ESMO open · Apr 2025 · ESMO Clinical Practice Guideline Express Update
metastatic pancreatic cancer
This is an ESMO clinical practice guideline express update addressing recent developments in managing metastatic pancreatic cancer. The update was issued following the approval of first-line nanoliposomal irinotecan (NALIRIFOX) and provides updated first- and second-line treatment recommendations and an updated management algorithm.
Key findings
- This ESMO Clinical Practice Guideline Express Update addresses developments in the management of metastatic pancreatic cancer.
- It has been issued following the approval of first-line nanoliposomal irinotecan (NALIRIFOX regimen).
- Updated first- and second-line treatment recommendations are provided.
- An updated management algorithm for metastatic pancreatic cancer is also included.
Limitations: Abstract-only summary of a guideline; no methodological details or evidence tables are provided in the abstract.; No primary patient-level data, sample sizes, or outcome measures are reported in the abstract.; No information on funding, conflicts of interest, or the strength/grade of specific recommendations is provided in the abstract..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text