Payment & Shipping Terms:
|Other Name:||2,4-DNP, 2,4-Dinitrofenol, Dinitra, Dinofan, Dinitrofenolo,||CAS:||51-28-5|
2,4-Dinitrobenzenol / 2, 4-Dinitrophenol / DNP / 51-28-5 inhibitor in
2,4-Dinitrophenol (DNP), C6H4N2O5, is a inhibitor of efficient energy (ATP) production in cells with mitochondria. It uncouples oxidative phosphorylation by carrying protons across the mitochondrial membrane, leading to a rapid consumption of energy without generation of ATP.
Dinitrophenols as a class of compounds, of which there are six members, do not occur naturally but are all manufactured compounds.
2,4-Dinitrophenol is a yellow, crystalline solid that has a sweet, musty odor. It sublimes when carefully heated and is volatile with steam. It is soluble in ethyl acetate, acetone, chloroform, pyridine, carbon tetrachloride, toluene, alcohol, benzene, and aqueous alkaline solutions. Its crystalline sodium salts are also soluble in water. It forms explosive salts with alkalies and ammonia, and emits toxic fumes of nitrogen oxides when heated to decomposition. It is incompatible with heavy metals and their compounds.
Commercial DNP is primarily used for scientific research and in manufacturing. It has been used at times to make dyes, other organic chemicals, and wood preservatives. It has also been used to make photographic developer, explosives, and pesticides.
In living cells, DNP acts as a proton ionophore, an agent that can shuttle protons (hydrogen cations) across biological membranes. It defeats the proton gradient across mitochondria and chloroplast membranes, collapsing the proton motive force that the cell uses to produce most of its ATP chemical energy. Instead of producing ATP, the energy of the proton gradient is lost as heat.
DNP is often used in biochemistry research to help explore the bioenergetics of chemiosmotic and other membrane transport processes.
DNP was used extensively in diet pills from 1933 to 1938 after Cutting and Tainter at Stanford University made their first report on the drug’s ability to greatly increase metabolic rate. After only its first year on the market Tainter estimated that probably at least 100,000 persons had been treated with DNP in the United States, in addition to many others abroad. DNP acts as a protonophore, allowing protons to leak across the inner mitochondrial membrane and thus bypass ATP synthase. This makes ATP energy production less efficient. In effect, part of the energy that is normally produced from cellular respiration is wasted as heat. The inefficiency is proportional to the dose of DNP that is taken. As the dose increases and energy production is made more inefficient, metabolic rate increases (and more fat is burned) in order to compensate for the inefficiency and meet energy demands. DNP is probably the best known agent for uncoupling oxidative phosphorylation. The production or “phosphorylation” of ATP by ATP synthase gets disconnected or “uncoupled” from oxidation. Interestingly, the factor that limits ever-increasing doses of DNP is not a lack of ATP energy production, but rather an excessive rise in body temperature due to the heat produced during uncoupling. Accordingly, DNP overdose will cause fatal hyperthermia. In light of this, it’s advised that the dose be slowly titrated according to personal tolerance, which varies greatly.Case reports have shown that an acute administration of 20–50 mg/kg in humans can be lethal. Concerns about dangerous side-effects and rapidly developing cataracts resulted in DNP being discontinued in the United States by the end of 1938. DNP, however, continues to be used by some bodybuilders and athletes to rapidly lose body fat. Fatal overdoses are rare, but are still reported on occasion. These include cases of accidental exposure, suicide, and excessive intentional exposure.
There are limited and conflicting data on the pharmacokinetics of DNP in humans. The EPA states that “Data on the elimination kinetics of the dinitrophenols or their metabolic products in humans were not found.” The ATSDR’s Toxicological Profile for Dinitrophenols also states that “No studies were located regarding distribution in humans after oral exposure to 2,4-DNP. Limited information is available regarding distribution in animals after oral exposure to 2,4-DNP.” However, they do state that “Elimination from the body appears to be rapid, except possibly in cases of compromised liver function.” This coincides with a review in the NEJM on the biological actions of dinitrophenol, which stated that “Judging from the metabolic response, DNP appears to be eliminated entirely in three or four days; in the presence of liver or kidney damage it is possible that the drug will be retained over a longer period.” Oddly, more recent papers give an array of possible half-lives, ranging from 3 hours, to 5–14 days.Other recent papers maintain that the half-life in humans is unknown.
Although further investigation is needed, one case report notes that dinitrophenol-induced hyperthermia has been successfully resolved with dantrolene administration. “Dinitrophenol uncouples oxidative phosphorylation, causes release of calcium from mitochondrial stores and prevents calcium re-uptake. This leads to free intracellular calcium and causes muscle contraction and hyperthermia. Dantrolene inhibits calcium release from the sarcoplasmic reticulum which reduces intracellular calcium. The resulting muscle relaxation allows heat dissipation. There is little risk to dantrolene administration. Since dantrolene may be effective in reducing hyperthermia caused by agents that inhibit oxidative phosphorylation, early administration may improve outcome.”
While DNP itself is considered by many to be too risky for human use, its mechanism of action remains under investigation as a potential approach for treating obesity. Currently, research is being conducted on uncoupling proteins naturally found in humans.
1. CAS No: 51-28-5
2. Molecular Formula: C6H4N2O5
3. Assay: 97.0%~103.0%
4. Appearance: Yellow powder .
5. Usage:can be used as pharmaceutical material,
2,4-Dinitrophenol is used in the manufacture of dyes, wood preservatives, and as a pesticide. The acute (short-term) effects of 2,4-dinitrophenol in humans through oral exposure are nausea, vomiting, sweating, dizziness, headaches, and loss of weight. Chronic (long-term) oral exposure to 2,4-dinitrophenol in humans has resulted in the formation of cataracts and skin lesions, weight loss, and has caused effects on the bone marrow, central nervous system (CNS), and cardiovascular system. Limited or no information is available on the developmental, reproductive, or carcinogenic effects of 2,4-dinitrophenol in humans. EPA has not classified 2,4-dinitrophenol for carcinogenicity.
2,4-Dinitrophenol (2,4-DNP, or simply DNP) is an organic compound with the formula HOC6H3(NO2)2. It is a yellow, crystalline solid that has a sweet, musty odor. It sublimes, is volatile with steam, and is soluble in most organic solvents as well as aqueous alkaline solutions. It is a precursor to other chemicals and is biochemically active, inhibiting energy (ATP) production in cells with mitochondria and was once used as a diet aid. It is produced by hydrolysis of 2,4-dinitrochlorobenzene.
DNP was used extensively in diet pills from 1933 to 1938 after Cutting and Tainter at Stanford University made their first report on the drug's ability to greatly increase metabolic rate. After only its first year on the market Tainter estimated that probably at least 100,000 persons had been treated with DNP in the United States, in addition to many others abroad. DNP acts as a protonophore, allowing protons to leak across the inner mitochondrial membrane and thus bypass ATP synthase. This makes ATP energy production less efficient. In effect, part of the energy that is normally produced from cellular respiration is wasted as heat. The inefficiency is proportional to the dose of DNP that is taken. As the dose increases and energy production is made more inefficient, metabolic rate increases (and more fat is burned) in order to compensate for the inefficiency and meet energy demands. DNP is probably the best known agent for uncoupling oxidative phosphorylation. The production or "phosphorylation" of ATP by ATP synthase gets disconnected or "uncoupled" from oxidation.
|Product name||2, 4-Dinitrophenol|
|CAS register number||51-28-5|
|Appearance||Buff monoclinic crystal powder .|
|Package||1kg/aluminium foil bag or as required|
|Minimum order quantity||10g|
|Shipping||By express courier|
|Shipping leading time||Within 24 hours after receiving the payment|
|Payment options||Western Union, MoneyGram, T/T|
1. Rich experience.
Our company is a professional production leading factory in China in pharmaceutical area of many years, our products have exported to Germany, Spain, UK, USA, Australia, Middle East, and so on other country, and we have got very good feedback from our customers, we had Established long friendly relations of cooperation. High quality, best price!
2. Great quality, purity and favourable.
Good quality is one of our secret success, welcome order the samples, MOQ just 10 grams.
3. Safe and fast delivery.
We have warehouse in Australia, Canada and England, we have large amounts of stock in the warehouse, can ship to you directly from our foreign warehouse! So we can delivery quickly at the very day when receive the payment. And We offer melting powder into liquid service.
4. Good after-sales service.
Tell the package update ASAP, and will try best solve when customer encountered various problems.