P1/2, N=30, Not yet recruiting, Lisata Therapeutics, Inc.

P1/2, N=50, Completed, Qilu Pharmaceutical Co., Ltd. | Recruiting --> Completed | Phase classification: P1b/2 --> P1/2 | Trial completion date: May 2023 --> Jun 2024 | Trial primary completion date: May 2023 --> Jun 2024

P2, N=120, Recruiting, Qilu Pharmaceutical Co., Ltd. | Not yet recruiting --> Recruiting

P1, N=0, Withdrawn, University of California, San Diego | N=21 --> 0 | Trial completion date: Dec 2029 --> Jun 2024 | Recruiting --> Withdrawn | Trial primary completion date: Dec 2028 --> Jun 2024

"Haystack Oncology...and Lisata Therapeutics...announced a research collaboration. Lisata will deploy the highly sensitive Haystack MRD technology for the detection of circulating tumor DNA (ctDNA) in a clinical study evaluating certepetide plus chemotherapy as an investigational treatment for metastatic pancreatic cancer. In the FORTIFIDE study, Lisata is investigating the safety, tolerability, and efficacy of its lead product candidate, certepetide...in subjects with metastatic pancreatic ductal adenocarcinoma (mPDAC) who have progressed on FOLFIRINOX, a treatment for pancreatic cancer. As part of this research, Lisata has engaged Haystack to use its MRD technology to measure serum ctDNA levels at multiple timepoints in patients throughout the study as an exploratory endpoint for analyzing the early therapeutic effect of certepetide."

P2, N=120, Not yet recruiting, Qilu Pharmaceutical Co., Ltd.

P2, N=155, Active, not recruiting, Australasian Gastro-Intestinal Cancer Trials Group | Recruiting --> Active, not recruiting

P2, N=80, Recruiting, Lisata Therapeutics, Inc. | N=120 --> 80

P2, N=120, Recruiting, Lisata Therapeutics, Inc.

P2, N=120, Recruiting, Lisata Therapeutics, Inc. | Phase classification: P2a --> P2

P2a, N=120, Recruiting, Lisata Therapeutics, Inc. | Trial completion date: May 2026 --> Dec 2025 | Trial primary completion date: May 2026 --> Dec 2025

Here we report the safety and efficacy results from a Phase Ib/II, multicenter study of LSTA1 plus (SoC) gemcitabine and locally produced nab-paclitaxel in patients with metastatic pancreatic ductal adenocarcinoma (mPDAC). LSTA1 combined with SoC showed an acceptable safety profile in patients with mPDAC. Compared with historical SoC data, LSTA1 plus SoC numerically improved ORR and PFS. Higher NRP1 expression is associated with better ORR and PFS, suggesting NRP1 may be a potential biomarker of LSTA1 plus chemotherapy for mPDAC treatment.

Under hypoxia, HIF-1α directly modulated NRP1 expression; HIF-1α silencing not only enhanced the anticancer effects of combined lenvatinib and hypoxia, but also prevented the loss of effectiveness caused by bafilomycin A1, highlighting the potential role of HIF-1α-derived hypoxia response in the adaptive cellular response to lenvatinib and promoting resistance acquisition by autophagy modulation. Overall, NRP1 may constitute a potential therapeutic target to prevent lenvatinib failure derived from a hypoxia-associated modulation of autophagy in advanced HCC.

From a mechanistic standpoint, this biological effect might rely on the expression of the β3 subunit integrin cell-extracellular matrix adhesive receptor. Our data, therefore, propose a reliable approach to explore invasive properties of patient glioma cells ex vivo and identify NRP1 as a mediator in this malignant process.

The duration of the tumor-penetrating effect of CEND-1 was evaluated by assessing tumor accumulation of Evans Blue and Doxorubicin in two different models of hepatocellular carcinoma (HCC): TGFα/c-myc-double transgenic mice and HepG2 xenografted mice. Conclusions These results indicate a favourable in vivo PK profile of CEND-1 after intravenous administration and demonstrate a specific and long-lasting tumour homing and tumor penetrability. Therefore, even single injections of CEND-1 may elicit long-lasting tumor PK improvements for co-administered anti-cancer agents.