Chlorophyll is a green pigment present in plants, as well as in eukaryotic single-celled algae and in several photosynthetic prokaryotes (the cyanobacteria and prochlorophytes), it plays crucial role in photosynthesis. The initial step in photosynthesis is the absorption of light by chlorophylls attached to proteins in the thylakoid membranes. Like cytochromes, chlorophylls consist of a porphyrin ring attached to a long hydrocarbon side chain. The energy of the absorbed light is used to remove electrons from an unwilling donor (water, in green plants), forming oxygen, and then to transfer the electrons to a primary electron acceptor, a quinone designated Q, which is similar to CoQ. Chlorophyll derivatives Radachlorin/Bremachlorin and Radachlorophyll/Bremachlorophyll are actually a second generation photosensitizer for photodynamic therapy of malignant and benign pathologies. Radachlorophyll/Bremachlorophyll may change blood lipids and pressure, including: (1) reduced total cholesterol; (2) increased HDL cholesterol; (3) reduced triglycerides; and (4) reduced systolic and diastolic blood pressure as well as immunomodulating properties. As a dietary supplement chlorophyll supports multiple body systems: provides antioxidant activity, supports vascular health, supports the body's normal immune system function, provides cardiovascular support, maintains skin and hair health. Chlorophylls (E140) is used as a food additive.

Angiotensin (1-7) [Ang 1-7] is a 7 amino acid peptide generated predominantly from Ang II by the action of Ang-converting enzyme 2. Ang 1-7 can act as a negative modulator of aldosterone secretion in vitro and in vivo. The endogenous heptapeptide angiotensin-(1-7) (Ang-(1-7)) is a RAS component that has a central role in the alternative axis. It is generated by the cleavage of Ang-II by the action of the angiotensin converting enzyme 2 (ACE 2) and acts via interaction with the G-protein coupled receptor Mas. Angiotensin (1-7) induces vasorelaxation through release of NO and prostaglandins, perhaps through activation of a non-AT1, non-AT2 receptor, Mas. Counteracts the vasoconstrictive and proliferative effects of angiotensin II and stimulates vasopressin (anti-diuretic hormone) release in vivo. Clinical uses range from treatment of cardiovascular-related diseases, ocular pathologies, metabolic dysfunctions, brain conditions and degenerative diseases to applications in cell differentiation and hematopoiesis, tumor therapy, acute lung injury, fibrosis, infection, among others. Tarix Orphan is developing TXA127 for rare neuromuscular and connective tissue diseases. TXA127 is a pharmaceutical formulation of the naturally occurring peptide, Angiotensin (1-7). TXA127 has been effective in animal models of Duchenne muscular dystrophy (DMD), Limb-girdle muscular dystrophy (LGMD), congenital muscular dystrophy MDC1A, Marfan syndrome, and Dystrophic Epidermolysis Bullosa (DEB). FDA granted rare pediatric disease designation to TXA127 from Tarix to treat recessive dystrophic epidermolysis bullosa (RDEB). TXA127 has been granted orphan drug status by FDA as a treatment for pulmonary arterial hypertension, to enhance engraftment in patients receiving a stem cell transplant, and for Myelodysplastic Syndrome (MDS). Tarix Orphan has broad IP protection for TXA127 and Orphan Drug Designations (ODDs) have been granted for DMD LGMD and DEB in the U.S., and for DMD in Europe. Tarix Orphan aims to initiate a clinical trials for both DMD and DEB in early 2018 and has an active IND for a Phase II trial in DMD, as well as Fast Track designation for DMD.

CMK is pyrrolopyrimidine derivatives that contained a chloromethyl ketone designed by the University of California. CMK shows potent irreversible inhibition of RSK2 protein kinase in mammalian cells.

RITA is anti-tumor agent that binds wild-type p53 (Kd = 1.5 nM) preventing p53-MDM2 (HDM2) interaction. Induces p53 accumulation and stimulates apoptosis in tumor cell lines expressing wild-type p53 in vitro and in vivo. Inhibits HPV-E6-mediated proteasomal degradation. RITA is well tolerated in mice after intraperitoneal administration, with no observable weight loss at doses up to 10 mg/kg during 1 month. After five injections of 0.1 mg/kg of RITA, the growth of the HCT116 tumors is suppressed by 40%, without apparent effects on the HCT116 TP53-/- tumors. At a dose of 1 or 10 mg/kg, RITA shows strong antitumor activity. Five 1 mg/kg injections of RITA results in a more than twofold decrease in the growth rate of p53-positive xenografts without any effect on p53-null xenografts. HCT116 tumors are 90% smaller in mice treated with 10 mg/kg of RITA than in control untreated mice. RITA inhibits the tumor growth in a wild-type p53−dependent manner.

NEO 212 is novel DNA alkylating agent exhibiting superior activity against breast cancer cells in vitro and intracranial triple-negative tumor growth in vivo. NEO212 is a conjugate of temozolomide (TMZ,) with the natural product perillyl alcohol (POH). NEO 212 causes DNA damage and cell death much more efficiently than TMZ because linkage with POH increased it's biological half-life and thus provided greater opportunity for placement of cytotoxic DNA lesions.

Metformin is the most widely used drug to treat type 2 diabetes, and is one of only two oral antidiabetic drugs on the World Health Organization (WHO) list of essential medicines. Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. However, we still do not completely understand its mechanisms of action. The main effect of this drug from the biguanide family is to acutely decrease hepatic glucose production, mostly through a mild and transient inhibition of the mitochondrial respiratory chain complex I. In addition, the resulting decrease in hepatic energy status activates AMPK (AMP-activated protein kinase), a cellular metabolic sensor, providing a generally accepted mechanism for the action of metformin on hepatic gluconeogenesis. The use of metformin, the most commonly prescribed drug for type 2 diabetes, was repeatedly associated with the decreased risk of the occurrence of various types of cancers, especially of pancreas and colon and hepatocellular carcinoma.

Metformin is the most widely used drug to treat type 2 diabetes, and is one of only two oral antidiabetic drugs on the World Health Organization (WHO) list of essential medicines. Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. However, we still do not completely understand its mechanisms of action. The main effect of this drug from the biguanide family is to acutely decrease hepatic glucose production, mostly through a mild and transient inhibition of the mitochondrial respiratory chain complex I. In addition, the resulting decrease in hepatic energy status activates AMPK (AMP-activated protein kinase), a cellular metabolic sensor, providing a generally accepted mechanism for the action of metformin on hepatic gluconeogenesis. The use of metformin, the most commonly prescribed drug for type 2 diabetes, was repeatedly associated with the decreased risk of the occurrence of various types of cancers, especially of pancreas and colon and hepatocellular carcinoma.

Metformin is the most widely used drug to treat type 2 diabetes, and is one of only two oral antidiabetic drugs on the World Health Organization (WHO) list of essential medicines. Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. However, we still do not completely understand its mechanisms of action. The main effect of this drug from the biguanide family is to acutely decrease hepatic glucose production, mostly through a mild and transient inhibition of the mitochondrial respiratory chain complex I. In addition, the resulting decrease in hepatic energy status activates AMPK (AMP-activated protein kinase), a cellular metabolic sensor, providing a generally accepted mechanism for the action of metformin on hepatic gluconeogenesis. The use of metformin, the most commonly prescribed drug for type 2 diabetes, was repeatedly associated with the decreased risk of the occurrence of various types of cancers, especially of pancreas and colon and hepatocellular carcinoma.

Fludeoxyglucose F-18 is a positron emitting radiopharmaceutical that is used for diagnostic purposes in conjunction with positron emission tomography (PET) imaging.

Pentaerythritol tetranitrate is an organic nitrate that has been used for the treatment of angina pectoris. Upon administration, the drug undergoes exstensive metabolism to NO which causes vasodilation and the relaxation of smooth muscle cells. The compound belongs to a familiy of explosive substances and may be used accordingly.