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Tuftsin

preclinical immune immune mass-verified
OOOOOONNNNNNNNHHHHHHHHHHHH
35 heavy atoms · 75 bonds · drag to pan, scroll to zoom C21N8O6

Skeletal structure drawn from the computed atomic coordinates in PubChem CID 156080. Carbons are implicit vertices; hydrogens on carbon are suppressed, as in any structural formula. Nothing here is estimated — every atom sits where PubChem placed it.

Research reference only. The observations below are recorded in the cited literature. Nothing here is advice or a recommendation, and no dosing information is published on this site.

Sequence

TKPR

Thr-Lys-Pro-Arg

1. Thr — Threonine · polar · hydropathy -0.7 · charge 0T12. Lys — Lysine · positive · hydropathy -3.9 · charge +1K3. Pro — Proline · proline · hydropathy -1.6 · charge 0P4. Arg — Arginine · positive · hydropathy -4.5 · charge +1R4

Computed backbone mass 500.6 Da agrees with PubChem's reported 500.6 Da (Δ 0.00 Da). Two independent sources agree on the primary structure.

Molecular data

Chemical fields come from the PubChem compound record; computed values are derived from the sequence shown above.
molecular formulaC21H40N8O6
molecular weight500.6 Da (PubChem)
computed backbone mass500.6 Da
length4 residues
net charge (pH 7.4)+2
mean hydropathy-2.67
half-lifenot characterised
delivery routenot characterised
PubChem CID156080
PDBnot characterised
UniProt parentP01859

Mechanism

Immunostimulatory tetrapeptide derived from the IgG heavy-chain Fc region.

Reported targets: neuropilin-1 phagocytes

Experimental structure

No experimental structure of this peptide is deposited in the PDB. Nothing is rendered here — a predicted fold would not be a structure, and this site does not draw one.

Position in the parent protein

exact match at residues 168–171 of Immunoglobulin heavy constant gamma 2 (395 aa)

…DVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNG…

Parent sequence from UniProt P01859. Tuftsin is released from the Fc region of IgG.

Reported effects

Each row is an outcome described in the literature indexed for this peptide. Reported in the cited work — not a claim, not a recommendation.

Reported observations and the corpus they are drawn from.
reported outcomewhere it appears
phagocyte stimulationFcγR-targeted tuftsin clusters rejuvenate macrophages in preclinical sepsis-… Science translational medicine 2025

Literature (8)

FcγR-targeted tuftsin clusters rejuvenate macrophages in preclinical sepsis-associated secondary infection — Science translational medicine 2025

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 41442500 · DOI 10.1126/scitranslmed.adv0313

Neuropilin-1-Targeted Cell-Penetrating Tandem Peptide-Drug Conjugate Exhibits Potent In Vivo Antiglioma and Antiangiogenic Activity — Journal of medicinal chemistry 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 42009314 · DOI 10.1021/acs.jmedchem.5c03835

An Engineered Multifunctional Fusion Protein Targeting Aβ Oligomers, Microglia and Autophagy Ameliorates Cognitive Deficits and Amyloid Pathology in Alzheimer's Disease Mice — Cellular and molecular neurobiology 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 42340476 · DOI 10.1007/s10571-026-01753-3

Antiproliferative Activity of the New Analogues of Acridine/Acridone With Oligopeptide Derivatives and Molecular Docking With EGFR and Src Kinase — Journal of peptide science : an official publication of the European Peptide Society 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 41382988 · DOI 10.1002/psc.70070

Tetrahedral DNA Nanostructure-Based Biomimetic Nanovesicles Attenuate Sepsis-Associated ARDS by Suppressing Glycolysis via the BMAL1/PFKFB3 Axis — Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2026

Sepsis-associated acute respiratory distress syndrome (SA-ARDS) is a life-threatening complication characterized by excessive pulmonary inflammation and pulmonary edema, lacking effective treatments. This study identifies the transcription factor BMAL1 in alveolar macrophages (AMs) as a key therapeutic target. Mechanistically, BMAL1 represses the expression of the glycolytic enzyme PFKFB3 by binding to the Pfkfb3 promoter, thereby inhibiting glycolysis, M1 polarization of AMs, and the generation of pro-inflammatory cytokines and reactive oxygen species (ROS). Based on this regulatory mechanism, a biomimetic nanoplatform, RM@TNT, is engineered for precise SA-ARDS therapy. Fabricated by hybridizing AM membrane-derived nanovesicles with ROS-responsive liposomes, the nanoplatform encapsulates tetrahedral DNA nanostructures (TNT) preloaded with nobiletin (Nob, a BMAL1 agonist) and Tuftsin (an…

open access ↗ · PMID 42003822 · DOI 10.1002/advs.202523782

Neuropilins in Multiple Sclerosis: Dual Roles of NRP-1 in Neuroinflammation and Neuroprotection — Neuromolecular medicine 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 42207333 · DOI 10.1007/s12017-026-08918-9

Correction to "The P2X7-Mediated Mitochondrial ROS as an Emerging Core Target of Tuftsin Nanoparticles in Severe Acute Pancreatitis Therapy via Regulating Mitophagy" — ACS applied materials & interfaces 2025

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 40619735 · DOI 10.1021/acsami.5c11986

The LRRK2 P1446L mutation triggers dopaminergic neurodegeneration via DAPK1-mediated microglial neuroinflammation and neuronal apoptosis — NPJ Parkinson's disease 2025

Parkinson's disease (PD) involves dopaminergic neuron loss and neuroinflammation, with leucine-rich repeat kinase 2 (LRRK2) mutations identified as major genetic risk factors. However, the pathogenic mechanism of the novel LRRK2-P1446L mutation remains unknown. Here, we designed LRRK2-P1446L mutant mice and demonstrated that the novel LRRK2-P1446L mutation drives neurodegeneration through death-associated protein kinase 1 (DAPK1) dysregulation. This mutation downregulates LRRK2 while upregulating DAPK1, which concurrently triggers microglial PI3K/Akt-dependent NF-κB activation (inducing IL-1β/IL-6/TNF-α expression) and neuronal mitochondrial apoptosis (via a Bax/Bcl-2 imbalance). Integrative multiomics revealed suppressed expression of the neuroprotective molecule tuftsin, which negatively correlated with DAPK1 expression and was linked to microbiota alterations. Our work establishes DAP…

open access ↗ · PMID 41423638 · DOI 10.1038/s41531-025-01234-2

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