DDInter1607 DDInter1678
Ritonavir is an HIV protease inhibitor that interferes with the reproductive cycle of HIV. Although it was initially developed as an independent antiviral agent, it has been shown to possess advantageous properties in combination regimens with low-dose ritonavir and other protease inhibitors. It is now more commonly used as a booster of other protease inhibitors and is available in both liquid formulations and as capsules. While ritonavir is not an active antiviral agent against hepatitis C virus (HCV) infection, it is added in combination therapies indicated for the treatment of HCV infections as a booster. Ritonavir is a potent CYP3A inhibitor that increases peak and trough plasma drug concentrations of other protease inhibitors such as and overall drug exposure. American Association for the Study of Liver Diseases (AASLD) and the Infectious Diseases Society of America (IDSA) guidelines recommend ritonavir-boosted combination therapies as first-line therapy for HCV Genotype 1a/b and
Sirolimus, also known as rapamycin, is a macrocyclic lactone antibiotic produced by bacteria _Streptomyces hygroscopicus_, which was isolated from the soil of the Vai Atari region of Rapa Nui (Easter Island). It was first isolated and identified as an antifungal agent with potent anticandida activity; however, after its potent antitumor and immunosuppressive activities were later discovered, it was extensively investigated as an immunosuppressive and antitumour agent. Its primary mechanism of action is the inhibition of the mammalian target of rapamycin (mTOR), which is a serine/threonine-specific protein kinase that regulates cell growth, proliferation, and survival. mTOR is an important therapeutic target for various diseases, as it was shown to regulate longevity and maintain normal glucose homeostasis. Targeting mTOR received more attention especially in cancer, as mTOR signalling pathways are constitutively activated in many types of human cancer. Sirolimus was first approved by the FDA in 1999 for the prophylaxis of organ rejection in patients aged 13 years and older receiving renal transplants. In November 2000, the drug was recognized by the European Agency as an alternative to calcineurin antagonists for maintenance therapy with corticosteroids. In May 2015, the FDA approved sirolimus for the treatment of patients with lymphangioleiomyomatosis. In November 2021, albumin-bound sirolimus for intravenous injection was approved by the FDA for the treatment of adults with locally advanced unresectable or metastatic malignant perivascular epithelioid cell tumour (PEComa). Sirolimus was also investigated in other cancers such as skin cancer, Kaposi’s Sarcoma, cutaneous T-cell lymphomas, and tuberous sclerosis. The topical formulation of sirolimus, marketed as HYFTOR, was approved by the FDA in April 2022: this marks the first topical treatment approved in the US for facial angiofibroma associated with tuberous sclerosis complex.
Ritonavir {u} (Compound) binds {v} (Gene) ABCB1
ABCB1 {u} (Gene) is bound by {v} (Compound) Sirolimus
Ritonavir {u} (Compound) downregulates {v} (Gene) VPS28
VPS28 {u} (Gene) is upregulated by {v} (Compound) Sirolimus
Ritonavir {u} (Compound) downregulates {v} (Gene) NT5DC2
NT5DC2 {u} (Gene) is downregulated by {v} (Compound) Sirolimus
Ritonavir {u} (Compound) causes {v} (Side Effect) Aspartate aminotransferase increased
Aspartate aminotransferase increased {u} (Side Effect) is caused by {v} (Compound) Sirolimus
Ritonavir {u} (Compound) resembles {v} (Compound) Atazanavir
Atazanavir {u} may lead to a major life threatening interaction when taken with {v} Sirolimus
Ritonavir {u} (Compound) binds {v} (Gene) ABCB1
ABCB1 {u} (Gene) is bound by {v} (Compound) Tacrolimus
Tacrolimus {u} (Compound) resembles {v} (Compound) Sirolimus
Ritonavir {u} (Compound) binds {v} (Gene) SLCO1B1
SLCO1B1 {u} (Gene) is bound by {v} (Compound) Estradiol
Estradiol {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Sirolimus
Ritonavir {u} (Compound) downregulates {v} (Gene) VPS28
VPS28 {u} (Gene) is downregulated by {v} (Compound) Everolimus
Everolimus {u} (Compound) resembles {v} (Compound) Sirolimus
Ritonavir {u} (Compound) downregulates {v} (Gene) NT5DC2
NT5DC2 {u} (Gene) is regulated by {v} (Gene) EAPP
EAPP {u} (Gene) is upregulated by {v} (Compound) Sirolimus
Ritonavir {u} (Compound) causes {v} (Side Effect) Aspartate aminotransferase increased
Aspartate aminotransferase increased {u} (Side Effect) is caused by {v} (Compound) Temsirolimus
Temsirolimus {u} (Compound) resembles {v} (Compound) Sirolimus
Ritonavir (Compound) binds ABCB1 (Gene) and ABCB1 (Gene) is bound by Sirolimus (Compound)
Ritonavir (Compound) downregulates VPS28 (Gene) and VPS28 (Gene) is upregulated by Sirolimus (Compound)
Ritonavir (Compound) downregulates NT5DC2 (Gene) and NT5DC2 (Gene) is downregulated by Sirolimus (Compound)
Ritonavir (Compound) causes Aspartate aminotransferase increased (Side Effect) and Aspartate aminotransferase increased (Side Effect) is caused by Sirolimus (Compound)
Ritonavir (Compound) resembles Atazanavir (Compound) and Atazanavir may lead to a major life threatening interaction when taken with Sirolimus
Ritonavir (Compound) binds ABCB1 (Gene) and ABCB1 (Gene) is bound by Tacrolimus (Compound) and Tacrolimus (Compound) resembles Sirolimus (Compound)
Ritonavir (Compound) binds SLCO1B1 (Gene) and SLCO1B1 (Gene) is bound by Estradiol (Compound) and Estradiol may cause a moderate interaction that could exacerbate diseases when taken with Sirolimus
Ritonavir (Compound) downregulates VPS28 (Gene) and VPS28 (Gene) is downregulated by Everolimus (Compound) and Everolimus (Compound) resembles Sirolimus (Compound)
Ritonavir (Compound) downregulates NT5DC2 (Gene) and NT5DC2 (Gene) is regulated by EAPP (Gene) and EAPP (Gene) is upregulated by Sirolimus (Compound)
Ritonavir (Compound) causes Aspartate aminotransferase increased (Side Effect) and Aspartate aminotransferase increased (Side Effect) is caused by Temsirolimus (Compound) and Temsirolimus (Compound) resembles Sirolimus (Compound)