Last update 01 Nov 2024

IL-15 x TIGIT

Last update 01 Nov 2024

Basic Info

Related Targets

IL-15TIGIT

Drugs associated with IL-15 x TIGIT

MFA-011

Target

IL-15 x TIGIT

Mechanism

IL-15 inhibitors [+1]

Active Org.

MediMabBio Co., Ltd.Startup

Originator Org.

MediMabBio Co., Ltd.Startup

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with IL-15 x TIGIT

100 Translational Medicine associated with IL-15 x TIGIT

0 Patents (Medical) associated with IL-15 x TIGIT

Literatures (Medical) associated with IL-15 x TIGIT

01 Mar 2024·Biomaterials

Dual-crosslinking immunostimulatory hydrogel synchronously suppresses pancreatic fistula and pancreatic cancer relapse post-resection

Article

Author: Zhao, Ruizhi ; Xiao, Qiuqun ; Zeng, Yinghua ; Zhang, Weiqi ; Zhan, Jie ; Fang, Chihua ; Cai, Yanbin ; Wu, Yuanyuan ; Liu, Jiale

In pancreatic cancer (PC), surgical resection remains the sole curative option, albeit patients undergoing resection are susceptible to postoperative pancreatic fistula (PF) formation and tumor recurrence. An unmet need exists for a unified strategy capable of concomitantly averting PF and tumor relapse to mitigate morbidity in PC patients after surgery. Herein, an original dual crosslinked biological sealant hydrogel (methacrylate-hyaluronic acid-dopamine (MA-HA-DA) and sulfhydryl-hyaluronic acid-dopamine (SH-HA-DA)) was engineered as a drug depot and loaded with polydopamine-cloaked cytokine interleukin-15 and platelets conjugated with anti-TIGIT. In vitro analyses validated favorable tissue adhesion, cytocompatibility, and stability of the hydrogels. In a PF rodent model, the hydrogel effectively adhered to the pancreatic stump, sealing the severed pancreatic end and impeding post-operative elevations in amylase and lipase. In PC murine models, hydrogels potently stimulated CD8⁺ T and NK cells to deter residual tumor re-growth and distant metastasis. This innovative hydrogel strategy establishes a new framework for concomitant prevention of PF and PC recurrence.

19 Feb 2024·Current Medicinal Chemistry

Evidence for the Involvement of Gene Regulation of Inflammatory Molecules in the Accumulation of Intracellular Cholesterol: The Mechanism of Foam Cell Formation in Atherosclerosis

Article

Author: Oishi, Yumiko ; Khotina, Victoria A ; Kolmychkova, Kira I ; Nikiforov, Nikita G ; Orekhov, Alexander N ; Borodko, Daria D ; Ekta, Mariam Bagheri ; Omelchenko, Andrey V ; Sukhorukov, Vasily N ; Sobenin, Igor A

Background:The relationship between the cellular pro-inflammatory response and intracellular lipid accumulation in atherosclerosis is not sufficiently studied. Transcriptomic analysis is one way to establish such a relationship. Previously, we identified 10 potential key genes (IL-15, CXCL8, PERK, IL-7, IL-7R, DUSP1, TIGIT, F2RL1, TSPYL2, and ANXA1) involved in cholesterol accumulation in macrophages. It should be noted that all these genes do not directly participate in cholesterol metabolism, but encode molecules related to inflammation.Methods:In this study, we conducted a knock-down of the 10 identified key genes using siRNA to determine their possible role in cholesterol accumulation in macrophages. To assess cholesterol accumulation, human monocyte-derived macrophages (MDM) were incubated with atherogenic LDL from patients with atherosclerosis. Cholesterol content was assessed by the enzymatic method. Differentially expressed genes were identified with DESeq2 analysis. Master genes were determined by the functional analysis.Results:We found that only 5 out of 10 genes (IL-15, PERK, IL-7, IL-7R, ANXA1) can affect intracellular lipid accumulation. Knock-down of the IL-15, PERK, and ANXA1 genes prevented lipid accumulation, while knock-down of the IL-7 and IL-7R genes led to increased intracellular lipid accumulation during incubation of MDM with atherogenic LDL. Seventeen overexpressed genes and 189 underexpressed genes were obtained in the DGE analysis, which allowed us to discover 20 upregulated and 86 downregulated metabolic pathways, a number of which are associated with chronic inflammation and insulin signaling. We also elucidated 13 master regulators of cholesterol accumulation that are immune response-associated genes.Conclusion:Thus, it was discovered that 5 inflammation-related master regulators may be involved in lipid accumulation in macrophages. Therefore, the pro-inflammatory response of macrophages may trigger foam cell formation rather than the other way around, where intracellular lipid accumulation causes an inflammatory response, as previously assumed.

01 Feb 2024·Future Oncology

The JAVELIN Bladder Medley Trial: Avelumab-Based Combinations as First-Line Maintenance in Advanced Urothelial Carcinoma

Article

Author: Hawley, Jessica ; Jacob, Natalia ; Hoffman-Censits, Jean ; Hahn, Noah M ; Mehr, Keyvan Tadjalli ; Seeberger, Sonja ; Guenther, Silke ; Grivas, Petros ; Powles, Thomas ; Tyroller, Karin

Results from JAVELIN Bladder 100 established avelumab (anti–PD-L1) first-line maintenance as the standard-of-care treatment for patients with advanced urothelial carcinoma (UC) that has not progressed with first-line platinum-based chemotherapy. We describe the design of JAVELIN Bladder Medley (NCT05327530), an ongoing phase II, multicenter, randomized, open-label, parallel-arm, umbrella trial. Overall, 252 patients with advanced UC who are progression-free following first-line platinum-based chemotherapy will be randomized 1:2:2:2 to receive maintenance therapy with avelumab alone (control group) or combined with sacituzumab govitecan (anti–Trop-2/topoisomerase inhibitor conjugate), M6223 (anti-TIGIT) or NKTR-255 (recombinant human IL-15). Primary end points are progression-free survival per investigator and safety/tolerability of the combination regimens. Secondary end points include overall survival, objective response and duration of response per investigator, and pharmacokinetics.

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