Nelfinavir is a protease inhibitor with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Nelfinavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Nelfinavir inhibits the HIV viral proteinase enzyme which prevents cleavage of the gag-pol polyprotein, resulting in noninfectious, immature viral particles. Nelfinavir is used in combination with other antiviral drugs in the treatment of HIV in both adults and children. Nelfinavir is marketed under the brand name Viracept.

Doxorubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Doxorubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Doxorubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. Doxorubicin is used to produce regression in disseminated neoplastic conditions like acute lymphoblastic leukemia, acute myeloblastic leukemia, Wilms’ tumor, neuroblastoma, soft tissue and bone sarcomas, breast carcinoma, ovarian carcinoma, transitional cell bladder carcinoma, thyroid carcinoma, gastric carcinoma, Hodgkin’s disease, malignant lymphoma and bronchogenic carcinoma in which the small cell histologic type is the most responsive compared to other cell types. Doxorubicin is also indicated for use as a component of adjuvant therapy in women with evidence of axillary lymph node involvement following resection of primary breast cancer.

Bufotalin is a cardiotoxic bufanolide steroid, cardiac glycoside analogue, secreted by a number of toad species; a novel anti-osteoblastoma agent. Bufotalin is a traditional Chinese medicine prepared from the dried secretion of the auricular and skin glands of Bufo bufo gargarizans Cantor. Bufotalin has drawn attentions from both cancer biologists and oncologists due to its dramatic antitumor activities. It has been shown that bufotalin inhibits cancer cell growth and induces cancer cell apoptosis in vivo and in vitro.

BMS-536924 is an ATP-competitive IGF-1R/IR inhibitor with IC50 of 100 nM/73 nM, modest activity for Mek, Fak, and Lck with very little activity for Akt1, MAPK1/2. BMS-536924 has been shown to inhibit the catalytic activity of IGF-1R and its down stream signaling components such as Akt and MAPK in cells; it also inhibits proliferation in a wide variety of human cancer cell lines including, colon, breast, lung, pancreas, prostate, sarcoma and multiple myeloma. In vivo, BMS-536924 inhibits tumor growth in an IGF-1R-dependent tumor model (IGF-1R Sal) as well as in a broad range of human tumor xenografts.

Beauvericin is a famous mycotoxin produced by many fungi, such as Beaveria bassiana and Fusarium spp. Beauvericin is a cyclic hexadepsipeptide (Figure 1) that belongs to the enniatin antibiotic family. It contains three D-hydroxyisovaleryl and three N-methylphenylalanyl residues in an alternating sequence. Beauvericin was first isolated from Beaveria bassiana, which is a common and commercial entomopathogenic mycoinsecticide. Beauvericin was one of the active constituents of B. bassiana and was confirmed to have antimicrobial and anti-tumor activities. Beauvericin has a strong antibacterial activity against human, animal and plant pathogenic bacteria with no selectively between Gram-positive and Gram-negative bacteria. The cytotoxicity of beauvericin to human tumor cells has been frequently reported.

Baccatin III is an isolate of the Pacific yew tree (Taxus brevifolia) and related species. Baccatin III is the precursor to paclitaxel/ taxol. Antileukaemic and antitumor agent, Baccatin III, binds to tubules when they are assembled in the cell and stabilizes the polymerized form of tubules so that they remain assembled even under conditions in which microtubules dissociate into tubulin subunits. Baccatin III is also an inducer of apoptosis and shows antitumor properties in vitro. Baccatin III exerts anti-tumor immunomodulatory activity in very low doses (0.05-0.5mg/kg), although it is regarded as an inactive derivative of paclitaxel. Oral administration of Baccatin III significantly reduced the growth of tumors induced by engrafting BALB/c mice with either 4 T1 mammary carcinoma or CT26 colon cancer cells. Baccatin III reduced tumor progression by inhibiting the accumulation and suppressive function of MDSCs. Baccatin III inhibited cell proliferation of a number of cancer cell lines. The cytotoxic activity exhibited by fungal taxol and Baccatin III involves the same mechanism, dependent on caspase-10 and membrane potential loss of mitochondria, with taxol having far greater cytotoxic potential.

Asiatic acid is a triterpene aglycone originally found in Centella; it exhibits cardioprotective, hepatoprotective, anti-inflammatory, antioxidative, antihypertensive, anticancer, anti-fibrotic, and anti-osteoporotic activities. In vitro and in vivo, asiatic acid inhibits TGF-β1-induced and overload-induced cardiac hypertrophy, decreasing production of TGF-β1 and activation of NF-κB, ERK1/2, and p38 MAPK. In high fat diet-fed rats, asiatic acid decreases expression of NF-κB, p38 MAPK, IL-1β, ROS, IL-6, and TNF-α and increases activity of glutathione peroxidase and catalase, preventing hepatic steatosis. Additionally, asiatic acid inhibits L-NAME-induced hypertension, increasing levels of NO and improving vascular function. In multiple myeloma cells, this compound induces G2/M phase cell cycle arrest, decreases expression of FAK, and inhibits cell proliferation. Asiatic acid inhibits adipogenesis, suppresses activation of G3PDH, and modulates differentiation in bone marrow stromal cells. In animal models of fibrosis, this compound decreases tubular injury and fibroblast activation by suppressing activation of Smad2/3, regulating PPARγ activation, and decreasing levels of α-SMA and TGF-β1. Asiatic acid stimulates wound healing by increasing collagen production. Asiatic acid is considered to be the most therapeutically active ingredient of Madecassol, marketed in Korea as wound healing agent for traumatic or surgical wounds, burns, skin grafts, fistulas, abnormal retractile or decubitus scars, cutaneomucous lesions in ENT, gynaecology, ulcerous lesions in leprosy, striae distensae, cellulitis, varicose leg ulcers, haemorrhoid.

Solasonine, a known glycoalkaloid, is a potential anti-cancer agent. Solasonine is a component of Curaderm BEC5 indicated for the topical treatment of actinic keratosis, keratoacanthoma, basal cell carcinoma and cutaneous superficial squamous cell carcinoma. BEC is a standardized mixture of Solamargine (33%), Solasonine (33%) and di-and monoglycosides of solasodine (34%) extracted from S. sodomaeum, now reclassified as S. linnaeanum. Solasonine could inhibit cell proliferation, migration and colony formation of glioma cells. Treatment of solasonine induced apoptosis via modulating cytochrome c and caspase signaling. Besides, solasonine decreased the expression of proinflammatory mediators and nuclear translocalization of NF-κB p50/p65. Mechanistic investigation further revealed that solasonine may target anti-inflammatory signaling pathway, and more specifically p-p38 and p-JNK MAPKs.

Nelfinavir is a protease inhibitor with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Nelfinavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Nelfinavir inhibits the HIV viral proteinase enzyme which prevents cleavage of the gag-pol polyprotein, resulting in noninfectious, immature viral particles. Nelfinavir is used in combination with other antiviral drugs in the treatment of HIV in both adults and children. Nelfinavir is marketed under the brand name Viracept.

Doxorubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Doxorubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Doxorubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. Doxorubicin is used to produce regression in disseminated neoplastic conditions like acute lymphoblastic leukemia, acute myeloblastic leukemia, Wilms’ tumor, neuroblastoma, soft tissue and bone sarcomas, breast carcinoma, ovarian carcinoma, transitional cell bladder carcinoma, thyroid carcinoma, gastric carcinoma, Hodgkin’s disease, malignant lymphoma and bronchogenic carcinoma in which the small cell histologic type is the most responsive compared to other cell types. Doxorubicin is also indicated for use as a component of adjuvant therapy in women with evidence of axillary lymph node involvement following resection of primary breast cancer.