Pharmaceutical Bulk Methylprednisolone Powder

CAS:83-43-2

MF: C22H30O5

MW:374.47

EINECS:201-476-4

Specification​: 99% min Methylprednisolone Powder

Sample: Methylprednisolone Powder

Packaging:1kg/bag, 25kg/drum

Brand: Henrikang

Appearance: White Powder

Storage: Cool Dry Place

Shelf Life: 2 Years

Test Method: HPLC

Levosulpiride Powder Usage and Synthesis.

Suitable for rheumatoid arthritis, collagen disease, allergic diseases, ophthalmic disorders, lymphatic leukaemia, soft tissue inflammation and haemolytic anaemia.

Inhibits virus-induced allergic reactions of the autoimmune system, thus reducing inflammation damage to lung cells; and effectively reduces fever, and is effective against urticaria vasculitis.

Uses and functions of Levosulpiride.

Stronger anti-inflammatory effect, weak effect on sodium retention, the same action as prednisone.

1. Methylhydroprednisone acetate suspension is slow to decompose and has a long-lasting effect, and can be injected intramuscularly or intra-articularly.

2. Methylhydroprednisone sodium succinate is water-soluble, can be injected into the muscle, or dissolved in glucose solution for intravenous drip. Because of the short half-life, it should be repeated after 4 hours for the treatment of severe shock.

Pharmacological Effects of Levosulpiride Raw.

Methylprednisolone is a synthetic glucocorticoid with typical glucocorticoid effects such as anti-inflammatory action and suppression of the immune response.

Compared with hydrocortisone, a representative of glucocorticoids, it has four times the anti-inflammatory efficacy of hydrocortisone, yet has only 80% of the effects of hydrocortisone. The half-life in plasma is 2.5 hours, and hydrocortisolone exhibits unfavourable and favourable effects depending on its clinical dosage and duration of treatment.

Production method of Bulk Levosulpiride Powder.

Methylprednisolone reduces RGC survival in rats with electrophysiologically diagnosed optic neuritis.

Methylprednisolone reduces RGC survival by a nongenomic, calcium-dependent mechanism.

Methylprednisolone-induced enhancement of RGC degeneration depends on calcium influx through voltage-gated calcium channels. In rostral and caudal stumps, Methylprednisolone treatment resulted in a significant reduction in the number of ED1-positive cells.

Methylprednisolone resulted in a significant reduction in tissue loss after treatments of 2, 4 and 8 weeks of injury.

After 1- and 2-week transition injuries, Methylprednisolone led to a long-term reduction in ED1-positive cells and spinal cord tissue loss, reduced vestibular fibre blight, and instantaneous sprouting of vestibular fibres adjacent to the lesion.

In a rat model of spinal cord injury, Methylprednisolone (30 mg/kg) effectively improved functional outcome, inhibiting TNF-α expression and NF-kB activation.Methylprednisolone inhibited the function of NF-kB, possibly induced by IKB, to trap NF-kB in the inactive cytoplasmic complex.