encephalomyelitis

Glatiramer acetate (GA) is a synthetic amino acid copolymer that is approved for treatment of relapsing remitting multiple sclerosis (RRMS) and clinically isolated syndrome (CIS).

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.

MOG (35-55) mouse, rat is a minor component of the central nervous system myelin with high brain specificity and strong immunogenicity. It can induce T and B cell responses, trigger relapsing-remitting neurological disorders with plaque-like demyelination, and is commonly used for inducing experimental autoimmune encephalomyelitis (EAE) models.

MOG peptide (35-55), mouse, rat acetate, is a minor component of central nervous system myelin with encephalitogenic activity. It can induce CD4⁺ T cell proliferation and Th1-type immune responses, leading to relapsing-remitting demyelinating disease. It is commonly used to establish experimental autoimmune encephalomyelitis (EAE) models.

LCKLSL hydrochloride is a hexapeptide compound and competitive inhibitor of membrane-bound protein A2 (AnxA2) with potential anti-angiogenic activity that inhibits the development of autoimmune encephalomyelitis (EAE) in mice.

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].

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].

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

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.

[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.

MOG (35-55) TFA is a minor component of central nervous system myelin with encephalitogenic activity. It can induce T cell proliferation, activate Th1 cytokine responses, and elicit high levels of IgG antibodies, leading to relapsing-remitting central nervous system disease characterized by extensive plaque-like demyelination. It is commonly used to induce experimental autoimmune encephalomyelitis (EAE) models.

PLP (139-151) is an amino acid fragment from positions 139 to 151 of myelin proteolipid protein (PLP), which is used to induce the relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE) model.

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.

Des-[Gly77,His78] Myelin Basic Protein (68-84) is a segment of the 68-84 sequence of guinea pig myelin basic protein (GPMBP). It influences the diversification of functions related to encephalitogenic and proliferative activities in T cells associated with experimental autoimmune encephalomyelitis (EAE).

Myelin basic protein, MBP (68-86), represents a segment from the 68th to the 86th amino acid residues in the MBP protein sequence. It can act as a self-antigen, initiating an immune response against the body’s own myelin sheath. Additionally, MBP (68-86) serves as an immunogen in experimental autoimmune encephalomyelitis (EAE) animal models and is utilized in studies concerning the immune responses linked to multiple sclerosis (MS).

IIIM1 is an orally active anti-inflammatory peptide. It alleviates symptoms of experimental autoimmune encephalomyelitis (EAE) by stimulating the proliferation of regulatory T cells and inducing them to produce RA1, which balances cytokine levels. IIIM1 is applicable for research on multiple sclerosis (MS).