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Showing 1 - 10 of 61356 pathways
SMPDB ID Pathway Chemical Compounds Proteins


Pw000270 View Pathway
drug action

Zoledronate Action Pathway

Homo sapiens
The action of zoledronate on bone tissue is based partly on its affinity for hydroxyapatite, which is part of the mineral matrix of bone. Zoledronate also targets farnesyl pyrophosphate (FPP) synthase. Nitrogen-containing bisphosphonates such as zoledronate appear to act as analogues of isoprenoid diphosphate lipids, thereby inhibiting FPP synthase, an enzyme in the mevalonate pathway. Inhibition of this enzyme in osteoclasts prevents the biosynthesis of isoprenoid lipids (FPP and GGPP) that are essential for the post-translational farnesylation and geranylgeranylation of small GTPase signalling proteins. This activity inhibits osteoclast activity and reduces bone resorption and turnover. In postmenopausal women, it reduces the elevated rate of bone turnover, leading to, on average, a net gain in bone mass.


Pw000724 View Pathway
drug action

Zidovudine Action Pathway

Homo sapiens
Zidovudine, a structural analog of thymidine, is a prodrug that must be phosphorylated to its active 5′-triphosphate metabolite, zidovudine triphosphate (ZDV-TP). It inhibits the activity of HIV-1 reverse transcriptase (RT) via DNA chain termination after incorporation of the nucleotide analogue. It competes with the natural substrate dGTP and incorporates itself into viral DNA.


Pw000195 View Pathway

Zellweger Syndrome

Homo sapiens
Zellweger syndrome (Cerebrohepatorenal syndrome; Cerebro-hepato-renal syndrome) phenotype is caused by mutations in any of several different genes involved in peroxisome biogenesis, Peroxins (PEX proteins, peroxisomal transport proteins) proteins 1,2,3,5,6,12,14, and 26. Peroxin proteins serve several functions including the recognition of cytoplasmic proteins that contain peroxisomal targeting signals (PTS) that tag them for transport by peroxismnal proteins to the peroxisome. Zellweger syndrome is characterized by accumulation of cholesterol in plasma, tissues and cerebrospinal fluid, decreased chenodeoxycholic acid and increased concentration of bile alcohols and their glyconjugates. Increased concentrations of cholestanol and apolipoprotein B are also observed in spinal fluid. Symptoms include dementia, psychiatric disturbances, pyramidal and/or cerebellar signs, and seizures.


Pw012895 View Pathway

Zeaxanthin Biosynthesis

Arabidopsis thaliana
Zeaxanthin biosynthesis is a pathway that occurs in the chloroplast by which lycopene becomes zeaxanthin, one of the most common carotenoid alcohols found in nature (Wikipedia). The first two reactions are catalyzed by lycopene beta cyclase which uses NAD(P)H as a cofactor to convert lycopene into gamma-carotene and gamma-carotene into beta-carotene. The last two reactions are catalyzed by beta-carotene 3-hydroxylase which uses ferredoxin and Fe2+ as cofactors to convert beta-carotene into beta-cryptoxanthin and beta-cryptoxanthin into zeaxanthin.


Pw000723 View Pathway
drug action

Zalcitabine Action Pathway

Homo sapiens
Zalcitabine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Within cells, zalcitabine is converted to its active metabolite, dideoxycytidine 5'-triphosphate (ddCTP), by the sequential action of cellular enzymes. ddCTP interferes with viral RNA-directed DNA polymerase (reverse transcriptase) by competing for utilization of the natural substrate deoxycytidine 5'-triphosphate (dCTP), as well as incorpating into viral DNA.


Pw002105 View Pathway

Xylose Degradation I

Escherichia coli
D-xylose, which can serve as a total source of carbon and energy for Escherichia coli K-12 substr. MG1655, enters the cell either through a low-affinity, proton-motive force-driven or a high-affinity, ATP-driven (ABC) transport system, so it is not phosphorylated during entry. Once inside the cell, an isomerase converts it to D-xylulose and subsequently a kinase converts it to D-xylulose 5-phosphate, an intermediate of the pentose phosphate pathway. Hence it flows through the pathways of central metabolism to satisfy the cell's need for precursor metabolites, reducing power, and metabolic energy. (EcoCyc)


Pw002433 View Pathway

xylitol degradation

Saccharomyces cerevisiae
The degradation of xylose begins with NADP dependent trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase resulting in the release of a NADPH, hydrogen ion and Xylitol. Xylitol reacts with a NAD D-xylulose reductase resulting in the release of NADH, a hydrogen ion and D-xylulose. Xylulose reacts with ATP through a xylulose kinase resulting in a release of ADP, hydrogen ion and xylulose 5-phosphate. The latter compound, xylulose 5-phosphate through a Ribulose-phosphate 3-epimerase resulting in the release of D-ribulose 5-phosphate. D-ribulose 5-phosphate and xylulose 5-phosphate react with a transketolase resulting in the release of D-glyceraldehyde 3-phosphate and D-sedoheptulose 7-phosphate. These two compounds react through a transaldolase resulting in the release of a D-erythrose 4-phosphate and Beta-D-fructofuranose 6-phosphate. D-erythrose 4-phosphate reacts with a xylulose 5-phosphate through a transketolase resulting in the release of Beta-D-fructofuranose 6-phosphate and D-glyceraldehyde 3-phosphate


Pw000301 View Pathway
drug action

Ximelagatran Action Pathway

Homo sapiens
Ximelagatran was the first member of the drug class of direct thrombin inhibitors that can be taken orally. It acts solely by inhibiting the actions of thrombin. Ximelagatran is a prodrug, being converted in vivo to the active agent melagatran.


Pw012896 View Pathway

Xanthophyll Cycle

Arabidopsis thaliana
The xanthophyll cycle consists of the conversions of zeaxanthin to antheraxanthin and violaxanthin. Xanthophylls are yellow pigments that occur widely in nature and form one of two major divisions of the carotenoid group (Wikipedia). Zeaxanthin epoxidase catalyzes the conversion of zeaxanthin to antheraxanthin and the conversion of antheraxanthin to violaxanthin. It requires FAD as a cofactor. Violaxanthin deepoxidase / antheraxanthin deepoxidase catalyzes the conversion of violaxanthin to antheraxanthin and the conversion of antheraxanthin to zeaxanthin.


Pw000489 View Pathway

Xanthinuria type II

Homo sapiens
Xanthinuria, also known as xanthine oxidase deficiency, is a rare genetic disorder causing the accumulation of xanthine. It is caused by a deficiency of the enzyme xanthine oxidase. Classic xanthinuria is a rare metabolic defect concerning the final reactions of purine catabolism. There are two types of the disorder: type I results from xanthine dehydrogenase (XDH) deficiency, while type II is characterized by lack of both XDH and aldehyde oxidase activity. Both types are clinically similar and are characterized by elevated xanthine concentration in body fluids that can lead to xanthine crystallisation. The most common manifestation of the disease is urolithiasis, but in most cases xanthinuria remains asymptomatic and the diagnosis is accidental.
Showing 1 - 10 of 61356 pathways