[5] The other medications used in combination include sofosbuvir, ribavirin, and interferon, vary depending on the virus type and whether the person has cirrhosis.

[5] Common side effects when used with sofusbivir and daclatasvir include headache, feeling tired, and nausea.

[4] With daclatasvir, sofosbuvir, and ribavirin the most common side effects are headache, feeling tired, nausea, and red blood cell breakdown.

[8] Daclatasvir is used only in combination therapy for the treatment of hepatitis C genotype 1, 3, or 4 infections; the agents used in combination, which include sofosbuvir, ribavirin, and interferon, vary based on the virus genotype, whether the person has cirrhosis and if a liver transplantation took place.

[4] Because it has not been extensively studied as a single agent, it is unknown what specific side effects are linked to this medication alone.

[4] Common adverse events occurring in >5% of people on combination therapy (sofosbuvir + daclatasvir) include headache and fatigue; in triple therapy (daclatasvir + sofosbuvir + ribavirin) the most common adverse events (>10%) include headache, fatigue, nausea and hemolytic anemia.

[4] Some common drugs that are strong CYP3A inducers include dexamethasone, phenytoin, carbamazepine, rifampin and St. John's Wort.

Currently, there are no required dosage adjustments with concurrent use of daclatasvir and immunosuppressants, narcotic analgesics, antidepressants, sedatives, and cardiovascular agents.

[12] Concurrent use with amiodarone, sofosbuvir and daclatasvir has may result in an increased risk for serious slowing of the heart rate.

[13] NS5A not only binds to cellular membranes, other non-structural proteins of the HCV replication-complex and viral RNA, but also to co-factors like PI4KA.

Concluding, daclatasvir presumably only inhibits PI4P hyper-accumulation in the context of full HCV polypeptide expression.

The second conformation of domain 1, which appears in non-treated cells, is then most likely to be associated with PI4P hyper-accumulation that is necessary for the formation and maintainment of the replication-complex and membranous web.

[17] The inhibition of hyper-accumulation of PI4P results in the collapse of the membranous web and the formation of large aggregated structures formed out of the proteins of the replication complex.

[16] Resulting from this observation, it is likely that the HCV replication-complex and virion hulls still get formed but are highly impaired by the treatment with daclatasvir.

[17] Furthermore, it has been observed, that the treatment of HCV infected cells with daclatasvir leads to a lack of the hyper-phosphorylated form of NS5A (p58).

[18] It was approved for use in Europe in August 2014, in the US in July 2015, and in India in December 2015; it was first in the class of NS5A inhibitors to reach the market.

[6] The daclatasvir molecule contains the two amino acids proline and valine in their natural L-form which makes it easier to synthesize in the right stereo configuration.

The dipeptide consists of the amino acids L-proline and L-valine and is solved in acetonitrile (MeCN).

[22] Daclatasvir has been tested in combination regimens with pegylated interferon and ribavirin,[23] as well as with other direct-acting antiviral agents including asunaprevir and sofosbuvir.