nadp+

NADP+ is the oxidized form of the electron donor nicotinamide adenine dinucleotide phosphate . It serves as a cofactor in various biological reactions. In addition, the balance between these reduced and oxidized forms plays key roles in diverse cellular functions, including cell survival, the maintenance of redox status, and intracellular signaling. For example, binding of NADP+ to β-subunits of Kv channels activates ion transport, whereas NADPH stabilizes channel inactivation. NADP+ is biosynthesized from NAD+ by NAD kinase, with ATP as the phosphoryl donor.

NADP disodium salt (Disodium NADP) is a nicotinamide adenine dinucleotide. NADP disodium salt is a key redox cofactor for electron transfer in the metabolism, serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH).

NADP sodium salt (Sodium NADP) is a coenzyme that is widely distributed in living matter. Participates in oxidation-reduction reactions.

Thio-NADP (S-NADP) functions as an inhibitor of nicotinic acid adenine dinucleotide phosphate (NAADP) and induces partial Ca 2+ release [1].

Niacin (Nicotinic acid) is a water-soluble vitamin belonging to the vitamin B family, which occurs in many animal and plant tissues, with antihyperlipidemic activity. Niacin is converted to its active form niacinamide, which is a component of the coenzymes nicotinamide adenine dinucleotide (NAD) and its phosphate form, NADP.

6-Aminonicotinamide (6-AN) is a well-established inhibitor of the NADP+-dependent enzyme.

Nicodan Percutan (Propylnicotinat) is the propyl ester form of niacin, which is found in various animal and plant tissues to form the coenzymes NAD and NADP.

Niacin hydrochloride is a water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is needed by the body for the formation of coenzymes NAD and NADP. It possesses PELLAGRA-curative, vasodilating, and antilipemic properties.

Galactose 1-dehydrogenase, pseudomonas fluorescens, a dehydrogenase found in Pseudomonas fluorescens, facilitates the oxidation of L-arabinose and D-galactose, utilizing NADP+ NAD+ as a cofactor. This enzyme is employed in diagnostic assays to quantify total galactose levels and serves as a biocatalyst in the production of galacturonic acid salts.

DA-11004 is a potent NADP-dependent isocitrate dehydrogenase inhibitor (IC50: 1.49 μM for IDPc). DA-11004 inhibited fatty acid synthesis in adipose tissues via IDPc inhibition. It also decreased the plasma glucose levels and FFA in HF diet-induced obesity

Glutathione can occur in reduced (GSH), oxidized (GSSG), or in mixed disulfide forms and is ubiquitous in multiple biological systems serving as the major thiol-disulfide redox buffer of the cell. GSSG is the oxidized form of GSH . It can be reduced back to GSH through the NADPH-dependent enzyme glutathione reductase. GSSG functions as a hydrogen acceptor in the enzymatic determination of NADP+ and NADPH and can be a proximal donor in S-glutathionylation post translational modifications. The ratio of reduced glutathione to oxidized glutathione within cells is often used as an indicator of oxidative stress, with higher concentrations of GSSG predicting increased oxidative stress.

Diminutol is a cell-permeable purine derivative that inhibits the NADP-dependent oxidoreductase, NQO1 (Ki = 1.72 μM), to destabilize microtubules and disrupt mitosis. At 50 μM, it directly affects tubulin polymerization in Xenopus egg extracts without interfering with the activity of Cdk1, DNA replication, or actin polymerization.

DNP-INT is a quinone analog that inhibits electron transport in plants by competitively inhibiting plastoquinol oxidation by binding at the Qo site of cytochrome b6f (Kd = 1.4 nM). It inhibits electron flow from water to NADP or methylviologen by 50 and 100% when used at concentrations of 0.5 or 5 μM, respectively.

DL-Glyceraldehyde (Glyceric aldehyde) is produced from the action of the enzyme glyceraldehyde dehydrogenase, which converts glycerol to glyceraldehyde using NADP as a cofactor. When present at sufficiently high levels, DL-Glyceraldehyde can be a cytotoxin and a mutagen. A cytotoxin is a compound that kills cells. A mutagen is a compound that causes mutations in DNA. DL-Glyceraldehyde is a highly reactive compound that can modify and cross-link proteins. DL-Glyceraldehyde modified proteins appear to be cytotoxic, depress intracellular glutathione levels, and induce reactive oxygen species (ROS) production (PMID: 14981296 ). DL-Glyceraldehyde has been shown to cause chromosome damage to human cells in culture and is mutagenic in the Ames bacterial test.

AS1134900 is a highly selective, non-competitive, metabotropic NADP+-dependent malic enzyme 1 (ME1) inhibitor.

1. Tuberostemonine (Tuberstemonine) exhibits relatively higher intestinal permeabilities. 2. Tuberostemonine acts in part as an open-channel blocker at the crayfish neuromuscular junction.

Isocitric acid (Isocitrate), an isomer of citric acid, is a substrate for citric acid cycle and an endogenous metabolite, which has potential for the treatment of Parkinson’s disease, Fe-deficiency anemia, and metabolic myopathies associated with a shortage of succinate dehydrogenase and aconitate hydratase, as well as the mutation of the gene of NADP-dependent isocitrate dehydrogenase 1 (IDH1).

D-Lactate dehydrogenase (D-LDH), an oxidoreductase, catalyzes the oxidation of D-lactate to pyruvate leveraging NAD+ or NADP+ as acceptors and acting on the donor CH-OH group. Predominantly found in bacteria and fungi, it is frequently utilized in biochemical research [1].

Glucose dehydrogenase (GDH) is an oxidoreductase enzyme that facilitates the oxidation of β-D-glucose into β-D-glucono-1,5-lactone, while concurrently reducing cofactor NADP+ to NADPH, and to a lesser degree, NAD+ to NADH. It can utilize both NAD+ and NADP+ as cofactors and serves in the regeneration of NADH and NADPH [1] [2].

Oxalomalic acid (Oxalomalate) trisodium, an inhibitor of aconitase and NADP-dependent isocitrate dehydrogenase, suppresses nitrite production and inducible nitric oxide synthase (iNOS) protein expression in lipopolysaccharide-activated J774 macrophages [1].

11β-13,14-Dihydro-15-keto PGF2α, a PGD2 metabolite in the 15-hydroxy PGDH pathway, is formed in human males upon infusion or inhalation of tritiated PGD2, with peak plasma levels of both 11β-PGF2α and 11β-13,14-dihydro-15-keto PGF2α observed within 10 minutes. In human lung homogenates, PGD2 is metabolized firstly to 11β-PGF2α and subsequently to 11β-15-keto-PGF2α in the presence of NAD+, but not to 11β-13,14-dihydro-15-keto PGF2α. Conversely, guinea pig liver and kidney homogenates can metabolize PGD2 to 11β-13,14-dihydro-15-keto PGF2α via 11β-PGF2α, with both NAD+ and NADP+ being requisite for this conversion.

PON-PC, an oxidized phospholipid with a 9-carbon fatty acyl chain ending in an aldehyde at the sn-2 position, arises from the oxidation of palmitoyl oleoyl phosphatidylcholine (POPC) or through interaction with ozone in pulmonary surfactant. It is found in oxidized LDL. At a 40 µM concentration, PON-PC diminishes the production of TNF-α, nitric oxide (NO), and NADP+ in primary mouse alveolar macrophages and lowers the bactericidal capability of RAW 264.7 cells. Additionally, levels of PON-PC increase in the bronchoalveolar lavage fluid (BALF) of mice exposed to cigarette smoke or in older mice.

IDE-IN-3 (Compound 4) serves as an inhibitor of Insulin-Degrading Enzyme (IDE). Computational predictions suggest that IDE-IN-3 potentially inhibits CYP3A4, CYP2C19, hERG, NADP+, HIF1α, and histidine kinase. This compound may exhibit biological activities in anti-diabetic, anti-tumor, and antibacterial applications.