mog (35 55), 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.

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

MART-1 (26-35) (human) (MART-1 (26-35) human) is a peptide fragment of MART-1 protein.

Myelin Oligodendrocyte Glycoprotein (MOG) peptide (35-55) , mouse, rat acetate is a MOG peptide (35-55) derivative. MOG peptide (35-55) is a part of myelin oligodendrocyte glycoprotein (MOG) immunogenic peptide and can be used to study immune-related diseases.

Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat (TFA) is a minor component of CNS myelin.

Prepro-Atrial Natriuretic Factor (26-55) (human) is a polypeptide that elevates cyclic GMP levels in the renal cortex and medulla and enhances renal guanylate cyclase activity [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].

β-Amyloid(28-35) human is a neurotoxic β-amyloid peptide fragment that contributes to Alzheimer's disease pathogenesis by interacting with neuronal membranes, modulating its secondary structure and toxicity. It also exhibits anisotropic effects on the acidic phospholipid DPH, thereby increasing the internal fluidity within lipid membrane bilayers [1].

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.

MART-1 (26-35) (human) TFA is an amino acid residue of 26-35 protein.

Amyloid-β (25-35) (Aβ (25-35)) is an 11-residue fragment of the Aβ protein that retains the physical and biological characteristics of the full length peptide. It forms fibrils that react to thioflavin T and Congo red and are organized in a cross-β arrangement of β-strands similar to Aβ (1-40) and Aβ (1-42) fibrils. Aggregated Aβ (25-35) decreases the viability of rat adrenal PC12 cells. It also decreases the viability of primary rat cortical neurons at concentrations ranging from 1 nM to 30 μM. In vivo, intracerebral injection of Aβ (25-35) (20 nmol) in rats induces lesions of neuronal and tissue loss. Aggregated Aβ (25-35) administered intracerebroventricularly to rats induces learning and memory impairments in the Y-maze, novel object recognition, and contextual fear conditioning tests.

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

CART(55-102)(human) TFA, a human satiety factor, exhibits strong appetite-suppressing activity. It is closely linked with leptin and neuropeptide Y [1] [2].

Human proinsulin, the single-chain peptide precursor of insulin, consists of the insulin A and B chains connected by the 31 amino acid C-peptide. Cleavage of proinsulin by proteolytic enzymes produces insulin and free C-peptide.

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.