[2] Common side effects include bone marrow suppression, vomiting, diarrhea, liver problems, rash, ulcer formation in the mouth, and bleeding.

[citation needed] Recently, cytarabine was reported to promote robust and persistent neuronal differentiation in NSC-34 motor neuron-like cell line.

Cytarabine is permissive, dispensable, and mostly irreversible in priming NSC-34 cells for neurite initiation and regeneration after mechanical dislodgement.

[citation needed] Toxicity: pancreatitis, leukopenia, thrombocytopenia, anemia, GI disturbances, stomatitis, conjunctivitis, pneumonitis, fever, and dermatitis, palmar-plantar erythrodysesthesia.

Rarely, myelopathy has been reported after high dose or frequent intrathecal Ara-C administration.

[21] The blockage of memory consolidation was proposed to be due to the inhibition by Ara-CTP of the DNA non-homologous end joining pathway.

[21] Thus transient DNA breakage followed by non-homologous end joining appear to be necessary steps in the formation of a long-term memory of an event.

[citation needed] Isolation of arabinose-containing nucleotides from the Caribbean sponge Cryptotheca crypta (now Tectitethya crypta) together with the realization that these compounds could act as DNA synthesis chain terminators led to exploration of these novel nucleotides as potential anticancer therapeutics.

[22] Cytarabine was first synthesized in 1959 by Richard Walwick, Walden Roberts, and Charles Dekker at the University of California, Berkeley.

[23] It was approved by the United States Food and Drug Administration in June 1969, and was initially marketed in the US by Upjohn under the brand name Cytosar-U.