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Related Concept Videos

Agonism and Antagonism: Quantification01:14

Agonism and Antagonism: Quantification

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When drugs are administered, they can elicit either an agonist or antagonist effect on the body. Agonism occurs when a drug activates a specific receptor, triggering a biological response. On the other hand, antagonism happens when a drug binds to the same receptors but blocks their activation, thereby preventing a biological response.
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Metallic Solids02:37

Metallic Solids

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Metallic solids such as crystals of copper, aluminum, and iron are formed by metal atoms. The structure of metallic crystals is often described as a uniform distribution of atomic nuclei within a “sea” of delocalized electrons. The atoms within such a metallic solid are held together by a unique force known as metallic bonding that gives rise to many useful and varied bulk properties.
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Structures of Solids02:22

Structures of Solids

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Solids in which the atoms, ions, or molecules are arranged in a definite repeating pattern are known as crystalline solids. Metals and ionic compounds typically form ordered, crystalline solids. A crystalline solid has a precise melting temperature because each atom or molecule of the same type is held in place with the same forces or energy. Amorphous solids or non-crystalline solids (or, sometimes, glasses) which lack an ordered internal structure and are randomly arranged. Substances that...
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Network Covalent Solids02:18

Network Covalent Solids

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Network covalent solids contain a three-dimensional network of covalently bonded atoms as found in the crystal structures of nonmetals like diamond, graphite, silicon, and some covalent compounds, such as silicon dioxide (sand) and silicon carbide (carborundum, the abrasive on sandpaper). Many minerals have networks of covalent bonds.
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Molecular and Ionic Solids02:54

Molecular and Ionic Solids

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Crystalline solids are divided into four types: molecular, ionic, metallic, and covalent network based on the type of constituent units and their interparticle interactions.
Molecular Solids
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Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

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Predictive Immune Modeling of Solid Tumors
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Predictive Immune Modeling of Solid Tumors

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Advancing ICOS agonism in solid tumors: lessons from INDUCE-1.

Parham Habibzadeh1, Diwakar Davar2

  • 1Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.

Journal for Immunotherapy of Cancer
|January 29, 2026
PubMed
Summary
This summary is machine-generated.

The inducible T-cell co-stimulator (ICOS) shows promise for immune therapy but requires precise targeting. Current ICOS agonists have limited clinical responses, indicating a need for combination strategies and biomarkers.

Keywords:
Immune Checkpoint Inhibitorco-inhibitory moleculeco-stimulatory molecules

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Use of Single Chain MHC Technology to Investigate Co-agonism in Human CD8+ T Cell Activation
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Area of Science:

  • Immunology
  • Oncology
  • Pharmacology

Background:

  • Inducible T-cell co-stimulator (ICOS) is a key immune regulatory molecule.
  • ICOS expression is upregulated upon T-cell activation, influencing immune responses.
  • ICOS interacts with other co-stimulatory pathways, making it a complex therapeutic target.

Purpose of the Study:

  • To evaluate the safety and biological activity of the ICOS agonist feladilimab in a Phase I study.
  • To explore the therapeutic potential of ICOS agonism in cancer immunotherapy.
  • To understand the factors limiting clinical efficacy of ICOS agonists.

Main Methods:

  • Phase I INDUCE-1 study utilizing a pharmacodynamically guided design.
  • Administration of feladilimab (GSK3359609) to assess safety and receptor occupancy.
  • Comparison with previous ICOS agonist studies, such as vopratelimab (JTX-2011).

Main Results:

  • Feladilimab demonstrated favorable safety and achieved robust receptor occupancy.
  • Clinical responses to feladilimab were limited, similar to other ICOS agonists.
  • Effective ICOS modulation requires careful consideration of T-cell responses and pathway interactions.

Conclusions:

  • ICOS agonism shows potential but faces challenges in achieving significant clinical efficacy.
  • Future strategies require combination therapies and biomarker-driven patient selection for ICOS-targeted treatments.
  • Optimizing ICOS modulation necessitates understanding spatial and temporal regulation of immune cell populations.