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

Peptide M acetate is a synthetic amino acid (18 amino acids in length which correspond to the amino acid positions 303-322 of bovine S-antigen: DTNLASSTIIKEGIDKTV). Peptide M acetate is capable of inducing experimental autoimmune uveitis in monkeys and Hartley guinea pigs as well as Lewis rats.

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

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].

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.

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.

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.

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].

MOG peptide (35-55), 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].

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].

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

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. It is noteworthy that mice subjected to MOG (92–106)-induced experimental autoimmune encephalomyelitis exhibit 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].

Ac-DEVD-CMK (Caspase-3 Inhibitor III) TFA is a selective and irreversible inhibitor of caspase-3, effectively preventing apoptosis triggered by elevated glucose levels or 3,20-dibenzoate (IDB). It is applicable in diverse experimental settings to impede apoptosis, as supported by references [1] [2] [3].

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.

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

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].

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.

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

[Leu144,Arg147]-PLP (139-151) is a mutated fragment of the myelin proteolipid protein (PLP), featuring substitutions of tryptophan to leucine and histidine to arginine at positions 144 and 147, respectively. Immunizing mice with this peptide (50 µg) mixed in complete Freund’s adjuvant (CFA) elevates IL-4 levels in the spleen. While it suppresses Th1 cell activation in vitro, it does not do so in vivo; instead, it promotes the development of regulatory T cells. Preimmunization with [Leu144, Arg147]-PLP (139-151) postpones the onset of experimental autoimmune encephalomyelitis (EAE) triggered by encephalitogenic peptides from PLP (178-191), myelin oligodendrocyte glycoprotein (MOG) (92-106), or myelin basic protein (MBP) in mice.

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

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].

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.

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.

IRBP (1-20), human TFA, features 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].

R 715, a bradykinin B1 receptor antagonist, inhibits contractions in isolated human umbilical cords that express bradykinin B1 receptors (pA2 = 8.49). When administered at doses of 200, 400, and 600 µg/kg, R 715 enhances latency to tail withdrawal in the tail-flick test for diabetic neuropathy mouse models induced by streptozotocin (STZ), signaling potential analgesic properties. Furthermore, at a 1 mg/kg per day dosage, it mitigates symptoms in a mouse model of experimental autoimmune encephalomyelitis (EAE) induced by MOG35-55 antigen peptide, such as reducing hind limb weakness and paralysis, improving gait symmetry, and decreasing spinal inflammation, neuron demyelination, and lesion monocyte invasion. Additionally, R 715 at 0.01 nmol/animal, administered intracerebroventricularly (i.c.v.), lowers mean arterial blood pressure and increases heart rate in spontaneously hypertensive rats, indicating cardiovascular effects.

Potent and selective KV1.3 channel blocker (IC50 values are 0.0019 and 0.65 nM for KV1.3 and KV1.1, respectively). Inhibits CD4+ CCR7- T cell activation. Ameliorates rat experimental autoimmune encephalomyelitis, in a model for multiple sclerosis.

he connecting segment 1 (CS-1) is a cell attachment domain located in the type III homology connecting segment (IIICS) of fibronectin. CS1 peptide of fibronectin, which lacks the Arg-Gly-Asp-containing domain, actively inhibits tumor metastases in spontan