通过降低 ROS 水平、下调细胞质 Nrf2 表达和上调全细胞 HO-1 表达，吡哆醇显示出其针对 AD 的保护潜力 [1]。

Absorption, Distribution and Excretion
The B vitamins are readily absorbed from the gastrointestinal tract, except in malabsorption syndromes. Pyridoxine is absorbed mainly in the jejunum. The Cmax of pyridoxine is achieved within 5.5 hours.
The major metabolite of pyridoxine, 4-pyridoxic acid, is inactive and is excreted in urine
Pyridoxine main active metabolite, pyridoxal 5’-phosphate, is released into the circulation (accounting for at least 60% of circulating vitamin B6) and is highly protein bound, primarily to albumin.

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Metabolism / Metabolites
Pyridoxine is a prodrug primarily metabolized in the liver. The metabolic scheme for pyridoxine is complex, with formation of primary and secondary metabolites along with interconversion back to pyridoxine. Pyridoxine's major metabolite is 4-pyridoxic acid.
Hepatic.
Half Life: 15-20 days

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Biological Half-Life
The total adult body pool consists of 16 to 25 mg of pyridoxine. Its half-life appears to be 15 to 20 days.

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Vitamin B6 (pyridoxine) is an essential nutrient in the human diet and is naturally found in human milk. Maternal supplementation increases milk levels in a dose-dependent manner. The recommended maternal minimum daily pyridoxine intake during pregnancy and lactation is 2 mg. The recommended adequate daily intake for neonates and infants up to 6 months of age is 0.1 mg. Intakes of 1 to 2 mg/kg pyridoxine daily are considered safe for neonates and infants receiving isoniazid for treatment or prevention of tuberculosis infection. Mothers taking a supplemental dose of 7.5 to 20 mg daily to prevent or treat B6 deficiency should have milk levels that provide an adequate B6 intake for the exclusively breastfed infant. Lower doses increase milk levels somewhat, but not necessarily sufficient. Higher doses of 100 to 200 mg daily used to prevent or treat some B6-responsive diseases have not been studied during lactation, but would not be expected to expose breastfed infants to a harmful amount. High-dose pyridoxine does not appear to be effective for lactation suppression.
◉ Effects in Breastfed Infants
Twenty postpartum women in Oklahoma were randomized to receive pyridoxine 2 mg or 27 mg once daily for 28 days beginning in the first postpartum week. One-half of the infants in the 2 mg maternal supplement group were given a daily multivitamin containing 0.4 mg pyridoxine, presumably started when breastfeeding was established, although this was not stated. Maternal dietary intakes of vitamin B6 during the study period were similar between the two groups. Weekly changes in weight and length Z scores were correlated with infant pyridoxine intake. Increases in weight and length Z scores over the course of the 28-day study period were similar between the directly supplemented infants and infants of mothers supplemented with 27 mg, and both were greater than nonsupplemented infants of mothers supplemented with 2 mg. However, these differences were clinically unimportant.
Seventeen postpartum lactating women in Indiana were given either a 2.5 mg or 15 mg daily pyridoxine supplement beginning on the day of hospital discharge and continued for 6 months, during which time their infants were exclusively breastfed. Prior to entering the study, all maternal participants had been taking routine prenatal vitamins containing vitamin B6 and had normal vitamin B6 status at baseline. In 15 of the infants, weight and length were measured at birth, and again at 1, 4, and 6 months postpartum. Both were similar between the two groups at all time points.
Forty-four term, healthy infants in Finland were prospectively followed for growth and vitamin B6 status beginning at birth and continuing through the first 12 months postpartum. All mothers followed World Health Organization guidelines at the time which involved exclusive breastfeeding for 6 months after birth, introducing supplemental solid foods at 6 months, and waiting to wean from breastfeeding until 9 months. At 12 months all the infants were still partly breastfed. All mothers were given a 1 mg pyridoxine supplement to take once daily beginning on postpartum day 5 and most took a pyridoxine supplement during pregnancy. Maternal vitamin B6 status was not reported. Seven of the 44 infants developed low B6 status during the first 6 months postpartum. Between 6 and 9 months those 7 infants had lower weight-for-age, and length grew more slowly than study infants with adequate status. By 10 to 12 months of age, there were no longer differences. This and other studies by the same group. suggest that exclusive breastfeeding carries a risk of infant low vitamin B6 status and poor growth, despite low-dose maternal supplementation.
A term, otherwise healthy newborn developed tremors in the arm, leg, and chin shortly after delivery. The infant had been put to breast one time prior to the onset of tremors. Biochemical tests of the infant’s blood were all within normal limits except their serum vitamin B6 was five times the upper normal limit. The mother’s serum vitamin B6 was twice the upper normal limit. The mother had been taking daily prenatal vitamins containing 4 mg of pyridoxine during pregnancy. Upon discontinuation of the maternal supplement, the infant’s serum B6 level decreased to near the upper normal limit within a month, symptoms gradually improved, and abnormal EEG findings at 2 months of age resolved by 6 months of age. Since the infant in this case only breastfed once and likely consumed only small amounts of colostrum, which has much lower levels of vitamin B6 than mature milk, this case likely involves vitamin B6 toxicity from transplacental exposure and not breastfeeding exposure. Considering the mother was not taking a high prenatal dose, this case also suggests some form of genetic variation in vitamin B6-dependent or metabolizing proteins in the mother and/or infant, which was not tested. Discontinuing maternal supplementation and reducing maternal dietary B6 intake, but continuing to breastfeed, is a reasonable approach in such a situation, since infant formula is likely to have a higher amount of vitamin B6.
◉ Effects on Lactation and Breastmilk
A systematic review found that two studies in the 1970s using very high maternal doses of 600 mg of pyridoxine daily in divided doses three times a day for 7 days begun shortly after delivery was effective at inhibiting lactation. However, these results have not been replicated in multiple other studies, nor has very high dose pyridoxine been demonstrated to reduce prolactin levels. A second systematic review found dopaminergic agents to be superior to pyridoxine in suppressing postpartum lactation.
A randomized, prospective, but nonmasked study compared cabergoline 1 mg (in one dose or 0.25 mg twice daily for 2 days; n = 45) to pyridoxine 200 mg 3 times daily for 7 days (n = 43) in suppressing lactation in postpartum women who did not wish to breastfeed. Treatment was initiated approximately 24 hours after delivery. Based on patient self-assessment, cabergoline was more effective than pyridoxine for suppressing lactation (78% vs 35%) and in reducing engorgement and pain (89% vs 67%) at day 7. The frequency of milk leakage was lower with cabergoline group after 7 and 14 days compared to pyridoxine (9% vs 42% and 11% vs 31%, , respectively). Headache and constipation were the most commonly reported adverse effects, occurring more frequently in cabergoline patients (15% vs 2%).

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Protein Binding
Pyridoxine main active metabolite, pyridoxal 5’-phosphate, is released into the circulation (accounting for at least 60% of circulating vitamin B6) and is highly protein bound, primarily to albumin.

[1]. Pyridoxine exerts antioxidant effects in cell model of Alzheimer's disease via the Nrf-2/HO-1 pathway. Cell Mol Biol (Noisy-le-grand). 2018 Jul 30;64(10):119-124.

Pyridoxine is a hydroxymethylpyridine with hydroxymethyl groups at positions 4 and 5, a hydroxy group at position 3 and a methyl group at position 2. The 4-methanol form of vitamin B6, it is converted intoto pyridoxal phosphate which is a coenzyme for synthesis of amino acids, neurotransmitters, sphingolipids and aminolevulinic acid. It has a role as a cofactor, a human metabolite, a Saccharomyces cerevisiae metabolite, an Escherichia coli metabolite and a mouse metabolite. It is a monohydroxypyridine, a vitamin B6, a member of methylpyridines and a hydroxymethylpyridine.
Pyridoxine is the 4-methanol form of vitamin B6, an important water-soluble vitamin that is naturally present in many foods. As its classification as a vitamin implies, Vitamin B6 (and pyridoxine) are essential nutrients required for normal functioning of many biological systems within the body. While many plants and microorganisms are able to synthesize pyridoxine through endogenous biological processes, animals must obtain it through their diet. More specifically, pyridoxine is converted to pyridoxal 5-phosphate in the body, which is an important coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, and aminolevulinic acid. It's important to note that Vitamin B6 is the collective term for a group of three related compounds, pyridoxine, pyridoxal, and pyridoxamine, and their phosphorylated derivatives, pyridoxine 5'-phosphate, pyridoxal 5'-phosphate and pyridoxamine 5'-phosphate. Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine. Vitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA). Pyridoxine is used medically for the treatment of vitamin B6 deficiency and for the prophylaxis of isoniazid-induced peripheral neuropathy (due to [DB00951]'s mechanism of action which competitively inhibits the action of pyridoxine in the above-mentioned metabolic functions). It is also used in combination with [DB00366] (as the commercially available product Diclectin) for the treatment of nausea and vomiting in pregnancy.
Pyridoxine is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
Pyridoxine is a Vitamin B6 Analog. The chemical classification of pyridoxine is Vitamin B 6, and Analogs/Derivatives.
Pyridoxine has been reported in Cyberlindnera jadinii, Glycine max, and other organisms with data available.
Pyridoxine is the 4-methanol form of vitamin B6 and is converted to pyridoxal 5-phosphate in the body. Pyridoxal 5-phosphate is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. Although pyridoxine and vitamin B6 are still frequently used as synonyms, especially by medical researchers, this practice is erroneous and sometimes misleading. Pyridoxine is one of the compounds that can be called vitamin B6. Pyridoxine assists in the balancing of sodium and potassium as well as promoting red blood cell production. It is linked to cancer immunity and helps fight the formation of homocysteine. It has been suggested that Pyridoxine might help children with learning difficulties, and may also prevent dandruff, eczema, and psoriasis. In addition, pyridoxine can help balance hormonal changes in women and aid in immune system. Lack of pyridoxine may cause anemia, nerve damage, seizures, skin problems, and sores in the mouth. Deficiency, though rare because of widespread distribution in foods, leads to the development of peripheral neuritis in adults and affects the central nervous system in children.
Pyridoxine is a metabolite found in or produced by Saccharomyces cerevisiae.
The 4-methanol form of VITAMIN B 6 which is converted to PYRIDOXAL PHOSPHATE which is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. Although pyridoxine and Vitamin B 6 are still frequently used as synonyms, especially by medical researchers, this practice is erroneous and sometimes misleading (EE Snell; Ann NY Acad Sci, vol 585 pg 1, 1990).
See also: Pyridoxine Hydrochloride (has salt form); Pyridoxine dipalmitate (is active moiety of); Broccoli (part of) ... View More ...

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Drug Indication
Pyridoxine is indicated for the treatment of vitamin B6 deficiency and for the prophylaxis of [DB00951]-induced peripheral neuropathy. It is also approved by Health Canada for the treatment of nausea and vomiting in pregnancy in a combination product with [DB00366] (as the commercially available product Diclectin).
FDA Label

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Mechanism of Action
Vitamin B6 is the collective term for a group of three related compounds, pyridoxine (PN), pyridoxal (PL) and pyridoxamine (PM), and their phosphorylated derivatives, pyridoxine 5'-phosphate (PNP), pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP). Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine. Vitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA).

C8H11NO3

169.1778

169.073

65-23-6

Pyridoxine-d5;688302-31-0;Pyridoxine hydrochloride;58-56-0

1054

White to off-white solid powder

1.4±0.1 g/cm3

491.9±40.0 °C at 760 mmHg

159-162ºC

251.3±27.3 °C

0.0±1.3 mmHg at 25°C

1.621

-1.1

73.58

3

4

2

12

142

0

LXNHXLLTXMVWPM-UHFFFAOYSA-N

InChI=1S/C8H11NO3/c1-5-8(12)7(4-11)6(3-10)2-9-5/h2,10-12H,3-4H2,1H3

4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~591.09 mM)

配方 1 中的溶解度: ≥ 2.08 mg/mL (12.29 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.08 mg/mL (12.29 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (12.29 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。