Publications by authors named "Inga Schapitz"

Chimeric antigen receptor (CAR)-T cell products, classified as Advanced Therapy Medicinal Products (ATMPs), have shown promising outcomes in cancer immunotherapy. The quality of raw and starting materials used in manufacturing is critical to ensure the efficacy and safety of CAR-T cell products and depends primarily on the selection of the right materials and the right suppliers. It is essential to consider a long-term strategy when selecting raw and starting materials to prevent delays in the supply of innovative, high-quality, and safe therapies to patients.

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Article Synopsis
  • To speed up the creation of Advanced Therapy Medicinal Products (ATMPs) for patients with serious cancers, regulatory strategies must be regularly reviewed and adapted, focusing on balancing risk with early clinical research.
  • The T2EVOLVE consortium is exploring ways to fast-track CAR and TCR-engineered T cell therapies in the EU by using existing regulatory tools to support an adaptable learning process for different product versions.
  • As knowledge about the connections between product quality, manufacturing, clinical effectiveness, and safety increases, there are emerging opportunities to simplify regulatory submissions and clinical studies, potentially applying these insights to other engineered cell therapies like CAR NK cell products.
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Atomistic descriptions of the μ-opioid receptor (μOR) noncovalently binding with two of its prototypical morphinan agonists, morphine (MOP) and hydromorphone (HMP), are investigated using molecular dynamics (MD) simulations. Subtle differences between the binding modes and hydration properties of MOP and HMP emerge from the calculations. Alchemical free energy perturbation calculations show qualitative agreement with in vitro experiments performed in this work: indeed, the binding free energy difference between MOP and HMP computed by forward and backward alchemical transformation is 1.

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Neuroligins are postsynaptic cell adhesion molecules that associate with presynaptic neurexins. Both factors form a transsynaptic connection, mediate signaling across the synapse, specify synaptic functions, and play a role in synapse formation. Neuroligin dysfunction impairs synaptic transmission, disrupts neuronal networks, and is thought to participate in cognitive diseases.

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