Quinacrine was initially developed as an anti-malarial drug marketed under the name Atabrine. Also it was approved for the teratment of ascites, however it was wothdrawn for both indication in 1995 and 2003, respectively. The drug is also used for the treatment of giardiasis, lupus, rheumatoid arthritis, refractory pulmonary effusion and pneumothorax, induce female sterilization etc. Proposed mechanisms of action include DNA intercalation interference with RNA transcription and translation, inhibition of succinate oxidation interference with electron transport, inhibition of cholinesterase, and inhibitor of phospholipase.

Cinchonine is cinchona bark alkaloid, which was used to treat malaria. Cinchonine is more efficient than quinine in increasing the intracellular accumulation and restoring the cytotoxicity of doxorubicin, mitoxantrone and vincristine on well-characterized multidrug resistance (MDR) cell lines. In the phase I of clinical trial was investigated the properties of cinchonine combined with the CHVP (cyclophosphamide, doxorubicin, vinblastine, methylprednisolone) regimen in relapsed and refractory lymphoproliferative syndromes.

Cinchonine is cinchona bark alkaloid, which was used to treat malaria. Cinchonine is more efficient than quinine in increasing the intracellular accumulation and restoring the cytotoxicity of doxorubicin, mitoxantrone and vincristine on well-characterized multidrug resistance (MDR) cell lines. In the phase I of clinical trial was investigated the properties of cinchonine combined with the CHVP (cyclophosphamide, doxorubicin, vinblastine, methylprednisolone) regimen in relapsed and refractory lymphoproliferative syndromes.

Cinchonine is cinchona bark alkaloid, which was used to treat malaria. Cinchonine is more efficient than quinine in increasing the intracellular accumulation and restoring the cytotoxicity of doxorubicin, mitoxantrone and vincristine on well-characterized multidrug resistance (MDR) cell lines. In the phase I of clinical trial was investigated the properties of cinchonine combined with the CHVP (cyclophosphamide, doxorubicin, vinblastine, methylprednisolone) regimen in relapsed and refractory lymphoproliferative syndromes.

Cinchonine is cinchona bark alkaloid, which was used to treat malaria. Cinchonine is more efficient than quinine in increasing the intracellular accumulation and restoring the cytotoxicity of doxorubicin, mitoxantrone and vincristine on well-characterized multidrug resistance (MDR) cell lines. In the phase I of clinical trial was investigated the properties of cinchonine combined with the CHVP (cyclophosphamide, doxorubicin, vinblastine, methylprednisolone) regimen in relapsed and refractory lymphoproliferative syndromes.

Cinchonine is cinchona bark alkaloid, which was used to treat malaria. Cinchonine is more efficient than quinine in increasing the intracellular accumulation and restoring the cytotoxicity of doxorubicin, mitoxantrone and vincristine on well-characterized multidrug resistance (MDR) cell lines. In the phase I of clinical trial was investigated the properties of cinchonine combined with the CHVP (cyclophosphamide, doxorubicin, vinblastine, methylprednisolone) regimen in relapsed and refractory lymphoproliferative syndromes.

Acriflavine (ACF) is a topical antiseptic. The hydrochloride form is more irritating than the neutral form. It is derived from acridine. Commercial preparations are often mixtures with proflavine. Acriflavine was developed in 1912 by Paul Ehrlich, a German medical researcher, and was used during the First World War against sleeping sickness. ACF has known trypanocidal, antibacterial, and antiviral activities. Effects of ACF on cancer cells were first reported 50 years ago. By present time was demonstrated that ACF a drug, that binds directly to HIF-1 alpha and HIF-2 alpha and inhibits HIF-1 dimerization and transcriptional activity and thus has potent inhibitory effects on tumor growth and vascularization. Also Acriflavine in combination with 3,6-diaminoacridine (proflavine) could prove to be a potential antimalarial drug and its pharmacological action can be due to inhibition of gyrase activity. This is achieved through interaction of the ACF with the DNA substrate. This interaction may lead to conformation change in DNA unsuitable for binding of gyrase with DNA.

Acriflavine (ACF) is a topical antiseptic. The hydrochloride form is more irritating than the neutral form. It is derived from acridine. Commercial preparations are often mixtures with proflavine. Acriflavine was developed in 1912 by Paul Ehrlich, a German medical researcher, and was used during the First World War against sleeping sickness. ACF has known trypanocidal, antibacterial, and antiviral activities. Effects of ACF on cancer cells were first reported 50 years ago. By present time was demonstrated that ACF a drug, that binds directly to HIF-1 alpha and HIF-2 alpha and inhibits HIF-1 dimerization and transcriptional activity and thus has potent inhibitory effects on tumor growth and vascularization. Also Acriflavine in combination with 3,6-diaminoacridine (proflavine) could prove to be a potential antimalarial drug and its pharmacological action can be due to inhibition of gyrase activity. This is achieved through interaction of the ACF with the DNA substrate. This interaction may lead to conformation change in DNA unsuitable for binding of gyrase with DNA.

Acriflavine (ACF) is a topical antiseptic. The hydrochloride form is more irritating than the neutral form. It is derived from acridine. Commercial preparations are often mixtures with proflavine. Acriflavine was developed in 1912 by Paul Ehrlich, a German medical researcher, and was used during the First World War against sleeping sickness. ACF has known trypanocidal, antibacterial, and antiviral activities. Effects of ACF on cancer cells were first reported 50 years ago. By present time was demonstrated that ACF a drug, that binds directly to HIF-1 alpha and HIF-2 alpha and inhibits HIF-1 dimerization and transcriptional activity and thus has potent inhibitory effects on tumor growth and vascularization. Also Acriflavine in combination with 3,6-diaminoacridine (proflavine) could prove to be a potential antimalarial drug and its pharmacological action can be due to inhibition of gyrase activity. This is achieved through interaction of the ACF with the DNA substrate. This interaction may lead to conformation change in DNA unsuitable for binding of gyrase with DNA.

Piperaquine is a bisquinoline antimalarial drug that was first synthesized in the 1960s and used extensively in China and Indochina as prophylaxis and treatment during the next 20 years. Usage declined in the 1980s as piperaquine-resistant strains of P. falciparum arose and artemisinin-based antimalarials became available. However, during the next decade, piperaquine was rediscovered by Chinese scientists as one of a number of compounds suitable for combination with an artemisinin derivative. The rationale for such artemisinin combination therapies (ACTs) was to provide an inexpensive, short-course treatment regimen with a high cure rate and good tolerability that would reduce transmission and protect against the development of parasite resistance. Piperaquine is characterized by slow absorption and a long biological half-life, making it a good partner drug with artemisinin derivatives which are fast acting but have a short biological half-life.