All terms in NCIT
| Label | Id | Description |
|---|---|---|
| CD16/IL15/CD33 Trispecific Killer Cell Engager | NCIT_C151948 | [A trispecific killer engager (TriKE) molecule containing an anti-cluster of differentiation 16 (CD16; FcgammaRIII) single-chain variable fragment (scFv) to engage natural killer (NK) cells, an anti-CD33 scFv to engage myeloid cells and a human modified interleukin-15 (IL-15) linker, that links the two scFv, with potential immunomodulating and antineoplastic activities against CD33-expressing tumor cells. Upon administration of the CD16/IL15/CD33 TriKE, the simultaneous binding to CD16 on NK cells and CD33 on tumor cells will induce NK cell cytotoxicity specifically against CD33-expressing tumor cells. The cytokine IL-15 linker promotes NK cell proliferation, activity, survival and expansion. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells.] |
| Percent Predicted Forced Inspiratory Volume in 1 Second | NCIT_C112380 | [The volume of air that a subject can breathe in during the first second of inhalation after maximum exhalation as a proportion of the predicted normal value. (CDISC)] |
| Vonoprazan Fumarate | NCIT_C151949 | [The fumarate salt form of vonoprazan, a pyrrole derivative and reversible potassium-competitive acid blocker (P-CAB), with potential antacid activity. Upon administration, vonoprazan specifically and competitively binds to the gastric hydrogen-potassium ATPase (H+/K+ ATPase) proton pump at or, more likely, near its potassium ion (K+) binding site and sterically inhibits K+ binding. This blocks the activation of the H+/K+ ATPase by K+, inhibits the proton pump and prevents gastric acid secretion, thereby lowering gastric acid levels.] |
| Cytoprotective Agent | NCIT_C2080 | [Agents administered before, with, or after cancer therapy to reduce or prevent damage or toxicity to the normal cells. (NCI)] |
| Anti-ulcer Agent | NCIT_C29701 | [Natural or synthetic Anti-ulcer Agents relieve and reduce the symptoms of ulcers in the stomach and upper small intestine, systemically and locally, by reducing gastric secretion (proton pump inhibitors), neutralizing hyperacidity (alkalinizing agents), or improving healing and protecting the mucosa (sucralfate). Recurrent gastric and duodenal ulcers caused by Helicobacter pylori infections are treated with antibiotic therapy.] |
| Percent Predicted Forced Vital Capacity | NCIT_C112381 | [Forced vital capacity as a proportion of the predicted normal value. (CDISC)] |
| Percent Predicted Inspiratory Capacity | NCIT_C112382 | [The maximum volume of air a subject can inhale into the lungs after a tidal exhalation (IRV plus TV) as a proportion of the predicted normal value. (CDISC)] |
| GJB2 Gene | NCIT_C126999 | [This gene plays a role in gap junction function.] |
| Restricted Diffusion | NCIT_C82346 | [Transport of substances across a biological membrane where the flux rate of the diffusing material is controlled by the permeability of the membrane, which in turn is dictated by the size of the pores.] |
| Hearing | NCIT_C16670 | [The auditory faculty, the perception of sound by the ear.] |
| Autologous PD1-inhibiting Anti-CD19 4-1BB CAR T Cells | NCIT_C151944 | [A preparation of autologous T-lymphocytes that are transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) linked to the intracellular signaling domain of 4-1BB (CD137) that also encodes a cell-intrinsic programmed cell death 1 (PD1; PDCD1; CD279; programmed death-1) short/small hairpin RNA (shRNA)-expressing cassette, with potential immunomodulating and antineoplastic activities. Upon administration of the autologous PD1-inhibiting anti-CD19 4-1BB CAR T-cells, these cells target, bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The shRNA silences expression of PD1, abrogates T-cell exhaustion, increases CAR T-cell activity and enhances tumor cytotoxicity. Expression of PD-1, an inhibitory receptor expressed on activated T-cells, plays a key role in CTL suppression, T-cell exhaustion and CTL apoptosis.] |
| IDO/TDO Inhibitor HTI-1090 | NCIT_C151945 | [An orally available inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1; IDO-1) and the kynurenine-producing hepatic enzyme tryptophan 2,3-dioxygenase (TDO), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1/TDO inhibitor HTI-1090 specifically targets and binds to both IDO1, a cytosolic enzyme responsible for the oxidation of the amino acid tryptophan into the immunosuppressive metabolite kynurenine, and TDO, a hepatic enzyme catalyzing the first step of tryptophan degradation. By inhibiting IDO1 and TDO, HTI-1090 decreases kynurenine levels in tumor cells, restores tryptophan and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells and T-lymphocytes. This reduces the number of tumor-associated regulatory T-cells (Tregs) and activates the immune system to induce a cytotoxic T-lymphocyte (CTL) response against the IDO1/TDO-expressing tumor cells, thereby inhibiting the growth of the tumor cells. IDO1 and TDO, both overexpressed by multiple tumor cell types, play important roles in immunosuppression and the promotion of tumor cell survival and proliferation. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.] |
| Topical Potassium Dobesilate | NCIT_C151946 | [A topical formulation composed of an inhibitor of fibroblast growth factor (FGF), with potential antineoplastic activity. Upon topical administration potassium dobesilate selectively binds to and blocks the activity of FGF, interferes with the binding of FGF to FGFR and prevents FGFR-mediated signaling. This inhibits angiogenesis and tumor cell proliferation, and induces cell death in FGFR-overexpressing tumor cells. FGF plays a key role in angiogenesis, tumor cell proliferation, survival and invasiveness, and is upregulated in many tumor cell types.] |
| Carcinogenesis Inhibition | NCIT_C15780 | [Suppression or prevention of the carcinogenic process/development of cancer.] |
| Anti-PD-L1 Monoclonal Antibody CK-301 | NCIT_C151947 | [An immunoglobulin G1 (IgG1), human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody CK-301 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death protein 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.] |
| Anti-PD-L1 Monoclonal Antibody | NCIT_C128057 | [A monoclonal antibody directed against programmed death-ligand 1 (PD-L1; CD274).] |
| Carcinogenesis Reversion | NCIT_C15781 | |
| GDF2 Gene | NCIT_C126995 | [This gene is involved in the inhibition of angiogenesis.] |
| Clinical Chemoprevention | NCIT_C15782 | [Chemoprevention use in a clinical setting.] |
| GDF2 wt Allele | NCIT_C126996 | [Human GDF2 wild-type allele is located in the vicinity of 10q11.22 and is approximately 5 kb in length. This allele, which encodes growth/differentiation factor 2 protein, plays a role in angiogenesis regulation. Mutation of the gene is associated with hereditary hemorrhagic telangiectasia type 5.] |