experimental

Experimental allergic encephalitogenic peptide (human), an EAE peptide, induces encephalomyelitis in guinea pigs [1].

CS1 peptide is present within type III homology connecting segment (IIICS) as well as C-274 (cell-binding domain). Fibronectin CS1 Peptide lacks the Arg-Gly-Asp-containing domain, actively inhibits tumor metastases in spontaneous and experimental metastas

Allylglycine is a glutamate decarboxylase inhibitor and a GAMMA-AMINOBUTYRIC ACID antagonist. It is used to induce convulsions in experimental animals.

FSL-1 TFA, a toll-like receptor 2/6 (TLR2/6) agonist derived from bacteria, bolsters resistance against experimental HSV-2 infection[1] and stimulates MMP-9 production via the TLR2 and NF-κB/AP-1 signaling pathways in monocytic THP-1 cells[2].

Z-LLE-AMC is a fluorogenic substrate for the caspase-like post-glutamate peptide hydrolase of the 26S proteasome or 20S proteolytic core. Caspase-like activity can be quantified by fluorescent detection of free AMC (also known as 7-amino-4-methylcoumarin), which is excited at 340-360 nm and emits at 440-460 nm. Z-LLE-AMC is typically used in cell lysates after experimental treatment.

Z-LLL-AMC is a fluorogenic substrate for the chymotrypsin-like activity of the 26S proteasome or 20S proteolytic core. Chymotrypsin-like activity can be quantified by fluorescent detection of free AMC (also known as 7-amino-4-methylcoumarin), which is excited at 340-360 nm and emits at 440-460 nm. Z-LLL-AMC is typically used in cell lysates after experimental treatment.

Certain chronic neurologic disorders, such as Parkinson's disease, are caused by an insufficiency of the neurotransmitter dopamine secondary to the degeneration of substantia nigra dopaminergic neurons. N-(α-Linolenoyl) tyrosine (NALT) is a simple α-amide conjugate between the ω-3 essential fatty acid α-linolenate and the amino acid tyrosine. α-Linolenate is an important precursor to docosahexaenoic acid (DHA), a prominent brain polyunsaturated fatty acid, while tyrosine is the metabolic precursor for neuronal dopamine synthesis. NALT was prepared as a method for enhancing central nervous system (CNS) dopamine content by facilitated transport of the tyrosine precursor across the blood-brain barrier. In experimental rat models of dopamine insufficiency, NALT increased CNS dopamine levels and exhibited an activity profile consistent with an anti-Parkinson's therapeutic agent.

MOG (35-55), human, a constituent of central nervous system myelin, is distinguishable from mMOG (35-55) due to a proline-to-serine substitution at position 42. It possesses immunogenic properties and is partially cross-reactive with mMOG35–55. However, MOG (35-55), human does not induce encephalitogenic effects, and only elicits minimal clinical signs of EAE (experimental autoimmune encephalomyelitis) in comparison to the rodent peptide.

Bovine Peripheral Myelin Protein P2 (53-78) is a derivative composed of amino acid residues 53 to 78 from the peripheral myelin P2 protein of bovine origin. It acts as a T cell epitope and is used to induce experimental autoimmune neuritis (EAN) in Lewis rats.

Ac-DEVD-CMK (Caspase-3 Inhibitor III) TFA is a selective, irreversible caspase-3 inhibitor, preventing apoptosis induced by elevated glucose levels or 3,20-dibenzoate (IDB) in various experimental contexts, as supported by references [1] [2] [3].

IRBP (1-20), human TFA, contains a prominent epitope recognized by the H-2b haplotype and is known to elicit experimental autoimmune uveoretinitis (EAU) in H-2b mouse models [1] [2].

MOG peptide (35-55) amide, a myelin oligodendrocyte glycoprotein (MOG) fragment spanning amino acids 35 to 55, selectively stimulates CD4+ T cell expansion and induces experimental autoimmune encephalomyelitis (EAE) in animal models [1] [2] [3].

Myosin H Chain Fragment, mouse, is a segment of the α-Myosin heavy chain peptide and serves as an inducer of experimental autoimmune myocarditis (EAM) in mouse models [1] [2].

Myosin H Chain Fragment, mouse acetate salt, a segment of the α-Myosin heavy chain peptide, is crucial for developing the experimental autoimmune myocarditis (EAM) mouse model [1] [2].

γ-Fibrinogen377-395 TFA is an inhibitory peptide derived from fibrinogen, which also functions as a fibrinogen epitope. It effectively blocks microglial activation and impedes fibrin-Mac-1 interactions in vitro. Additionally, it exhibits in vivo efficacy by suppressing experimental autoimmune encephalomyelitis (EAE) in mice. This compound has applications in researching multiple sclerosis (MS) and other neuroinflammatory diseases linked to blood-brain barrier disruption and microglial activation [1].

γ-Fibrinogen377-395 is a peptide derived from fibrinogen, functioning both as an inhibitory molecule and an epitope. It inhibits microglial activation, disrupts fibrin-Mac-1 interactions in vitro, and mitigates experimental autoimmune encephalomyelitis (EAE) in murine models in vivo. This compound is relevant for research into multiple sclerosis (MS) and other neuroinflammatory disorders characterized by blood-brain barrier compromise and microglial activation [1].

Myelin Basic Protein (1-11), an encephalitogenic epitope of MBP, facilitates the induction of experimental autoimmune encephalomyelitis (EAE) [1] [2].

MOG (92–106), mouse, rat, is a biologically active peptide corresponding to the fragment of amino acids 92 to 106 in myelin oligodendrocyte glycoprotein (MOG) from mice and rats. Mice subjected to MOG (92–106)-induced experimental autoimmune encephalomyelitis show substantial B cell reactivity to secondary myelin antigens. Although this MOG fragment elicits only modest T cell responses, the resultant autoimmunity is profoundly severe. The peptide demonstrates encephalitogenic properties in various species, including SJL mice, DA rats, and rhesus monkeys.

J5 peptide, an MBP inhibitor, competitively inhibits the binding of MBP 85-99 to HLA-DR2, and mitigates PLP 139-151 MBP 85-99-induced experimental autoimmune encephalomyelitis (EAE) in mice. It is utilized in research pertaining to inflammatory and immune diseases [1].

IRBP-derived peptide R16, an active biological peptide, is a segment of the interphotoreceptor retinoid-binding protein (IRBP) known to induce experimental autoimmune uveitis (EAU) in susceptible animal strains.

R16, an interphotoreceptor retinoid binding protein (IRBP)-derived peptide, exhibits biological activity with the capability to induce experimental autoimmune uveitis (EAU) in susceptible animal strains as a photoreceptor cell protein.

Antiarrhythmic peptide (cattle atrium), a hexapeptide, exhibits a protective effect against experimentally induced arrhythmias [1].

AChRα(97-116), a peptide implicated in the induction of experimental autoimmune myasthenia gravis (EAMG), serves as a targeted agent in this autoimmune disorder [1].

Ac2-12 TFA, an annexin lipocortin 1 (LC1)-mimetic peptide, inhibits neutrophil extravasation and demonstrates antimigratory effects by attenuating the recruitment of neutrophils in experimental models of inflammation [1] [2].