M-AMSA

M-AMSA Uses, Dosage, Side Effects, Food Interaction and all others data.

Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects.

M-AMSA is an aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects.

M-AMSA
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
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Interaction With other Medicine
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Trade Name	M-AMSA
Generic	Amsacrine
Amsacrine Other Names	Acridinyl anisidide, Amsacrina, Amsacrine, Amsacrinum, m-AMSA, mAMSA
Type
Formula	C₂₁H₁₉N₃O₃S
Weight	Average: 393.459 Monoisotopic: 393.114712179
Protein binding	96-98%
Groups	Approved, Investigational
Therapeutic Class
Manufacturer
Available Country
Last Updated:	September 19, 2023 at 7:00 am

Uses

M-AMSA is a cytotoxic agent used to induce remission in acute adult leukemia that is not adequately responsive to other agents.

For treatment of acute myeloid leukaemia.

M-AMSA is also used to associated treatment for these conditions: Leukemia, Acute, Refractory Leukemia

How M-AMSA works

M-AMSA binds to DNA through intercalation and external binding. It has a base specificity for A-T pairs. Rapidly dividing cells are two to four times more sensitive to amsacrine than are resting cells. M-AMSA appears to cleave DNA by inducing double stranded breaks. M-AMSA also targets and inhibits topoisomerase II. Cytotoxicity is greatest during the S phase of the cell cycle when topoisomerase levels are at a maximum.