mog , human

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 (89-113), human is a peptide fragment of human myelin oligodendrocyte glycoprotein.

Myelin oligodendrocyte glycoprotein (MOG) peptide, a truncated form of MOG located on the extracellular myelin sheath surface, interacts with antigen serotype HLA-DR2 to mitigate effects of ischemic stroke induced by middle cerebral artery occlusion (MCAO) in mice. In female mice, it notably reduces cortical and striatal infarct volumes, lessens sensorimotor deficits as observed in tube- and corner turn tests, enhances engagement with novel odors, and prolongs the duration of cage mate-directed vocalizations, without exhibiting similar outcomes in male mice.

Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat (MOG (35-55)) is a truncated peptide derived from the human Myelin Oligodendrocyte Glycoprotein (MOG).

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.