exocytosis

PFM03 is an endonuclease inhibitor that specifically blocks Mre11 and is also able to reduce MRN endonuclease activity by 98%, blocking hMRN-mediated endonucleotomy and nuclear exocytosis processes on the protein-binding end of the 5 ' and 3 ' chains.

Vacuolin-1 is a cell-permeable inhibitor of Ca2+ dependent fusion of lysosomes to the cell membrane. It acts by inhibiting release of lysosomal content.vacuolin‐1 is a potent and selective PIKfyve inhibitor and inhibits late‐stage autophagy by impairing lysosomal maturation

Antagonist of formyl peptide receptor 1 (FPR1). Reduces superoxide production induced by fMLF with an EC50 of 0.63 μM. Almost completely blocks fMLF-stimulated primary granule exocytosis.

fMIFL is an FPR1 agonist that activates several transduction pathways responsible for various neutrophil functions, such as adhesion, chemotaxis, granule secretion through exocytosis, and the production of superoxide anions. It is used in the research of bacterial infections and tissue damage.

FFN200 is a vesicular monoamine transporter 2 (VMAT2) substrate that selectively traces monoamine exocytosis in both neuronal cell culture and brain tissue.

Endosidin5 is a novel exocytosis inhibitor.

ω-Agatoxin IVA TFA is a potent selective inhibitor of P Q type Ca2+ (Cav2.1) channels, with IC50 values of 2 nM for P-type and 90 nM for Q-type channels. It effectively inhibits glutamate exocytosis and calcium influx induced by high potassium, with IC50 values ranging from 30 to 225 nM. Additionally, it blocks high potassium-induced serotonin and norepinephrine release, without impacting L-type or N-type calcium channels [1][2].

TAT-NSF700scr comprises the complete TAT domain and a glycine linker, succeeded by the NSF amino acids arranged randomly. It serves as a control peptide, ineffective in inhibiting SNARE-mediated exocytosis [1] [2].

TAT-NSF222 Fusion Peptide is a bifunctional polypeptide comprising a TAT domain for cellular uptake via macropinocytosis and an NSF domain that inhibits N-ethylmaleimide-sensitive factor (NSF), serving as an exocytosis inhibitor [1].

α-Latrotoxin, a potent neurotoxin derived from black widow spider venom, induces synaptic vesicle exocytosis at presynaptic nerve terminals [1].

This amino acids187 to 203 fragment is derived from the C-terminal helix of synaptosomal-associated protein of 25 kDa (SNAP-25). This peptide is able to rescue exocytosis from botulinum neurotoxin E (BoNT/E)-treated cells, albeit at higher concentrations

ARF1 (2-17) inhibits both ARF-dependent (i.e., PLD) and ARF-independent pathways (i.e., PLC-β). This compound also suppresses GTP-γ-S-stimulated PLD activity, phospholipase C-β (PLC-β), and exocytosis.