与正常乳腺上皮 (MCF-12A) 细胞相比，生物素对乳腺癌 (T47D) 细胞表现出更高的亲和力，Kms 值分别为 9.24 μM 和 53.1 μM [4]。 T47D 细胞对生物素的吸收具有剂量依赖性（0.09-100 μM；0-70 分钟），Vmax 为 27.34 pmol/mg 蛋白质/分钟 [4]。细胞粘附力降低，生物素（1-1000 nM；24 小时）部分恢复 7β-OHC (50 µM) 诱导的细胞死亡 [5]。

在给予链脲佐菌素（150 mg/kg；腹腔注射）以产生糖尿病的大鼠中，生物素（15 mg/kg/d；口服；12 天）可降低肾毒性[6]。生物素水平不足（0.012 mg/kg/d；口服；70 天）的鱼的大脑、脾脏和皮肤的免疫活性受损[7]。

细胞活力测定 [5]
细胞类型： 小鼠少突胶质细胞 158N 细胞
测试浓度： 1、10、100、1000 nM
孵育持续时间：24小时
实验结果：显示细胞保护作用并防止7β-羟基胆固醇诱导的氧化还原态破坏。改善氧化应激、线粒体功能障碍和脂质代谢变化的衰减。

Animal/Disease Models: Streptozotocin-induced male Swiss albino mice (25±2 g) [6]
Doses: 15 mg/kg/d
Route of Administration: po (oral gavage); 12-day
Experimental Results: Improved histopathological results, Includes distorted glomeruli, inflammatory cells, and macrophages, and reduces the acrylate response to oxidative damage.

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Animal/Disease Models: grass carp (117±0.5 g) [7]
Doses: 0.012, 0.110, 0.214, 0.311, 0.427 and 0.518 mg/kg
Route of Administration: po (oral gavage); 70-day
Experimental Results: Lysozyme (LZ) and acid phosphatase (ACP) activity is diminished, and the levels of complement 3 (C3), C4 and immunoglobulin M (IgM) are diminished. Decreases the mRNA levels of antimicrobial substances. It partially increases the mRNA levels of pro-inflammatory cytokines and tumor necrosis factor, partially reduces the levels of anti-inflammatory IL-4/13A, IL-10, IL-11 and TGF-β1 mRNA, and partially interacts with target of rapamycin (TOR) signaling. Conduction related.

Absorption, Distribution and Excretion
Systemic - approximately 50%
The intestine is exposed to biotin from a few sources: the diet, biotin supplements and biotin synthesized by bacteria in the large intestine. Dietary biotin exists in free and protein-bound forms. Protein-bound biotin is digested by proteases and peptidases to biotin-containing oligopeptides and biocytin (epsilon-N-biotinyl-L-lysine). Biocytin and the biotin-containing oligopeptides are converted to biotin via the enzyme biotinidase. Biotin - both dietary-derived biotin and supplementary biotin - is efficiently absorbed from the small intestine. At doses of biotin derived from food, biotin appears to be transported into enterocytes by a sodium -dependent carrier. At higher doses of biotin,absorption appears to occur by passive diffusion. Absorption of the biotin produced by the colonic microflora, appears to occur by a carrier mediated process in the proximal large intestine.
Elimination: Primarily in urine.
Protein binding: Primarily to plasma proteins.
Absorption: approximately 50%.
For more Absorption, Distribution and Excretion (Complete) data for BIOTIN (32 total), please visit the HSDB record page.

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Metabolism / Metabolites
Biotin is excreted in the urine as biotin, bisnorbiotin, biotin sulfoxide, biotin sulfone, bisnorbiotin methyl ketone and tetranobiotin-1-sulfoxide.
Biotin is catabolized to a number of different metabolites, including bisnorbiotin, biotin sulfoxide, biotin sulfone, bisonorbiotin methylketone and tetranorbiotin-1-sulfoxide.
More than 95% of the biotin is free in the skim fraction of human milk. The concentration of biotin varies substantially in some women and exceeds that in serum by one to two order of magnitude, suggesting that there is a transport system into milk. The biotin metabolite bisnorbiotin accounts for approximately 50%. In early and transitional human milk, the biotin metabolite biotin sulfoxide accounts for about 10% of the total biotin plus metabolites. With postpartum maturation, the biotin concentration increases, but the bisnorbiotin and biotin sulfoxide concentrations still account for 25% and 8% at 5 weeks postpartum. Current studies provide no evidence for a soluble biotin-binding protein or any other mechanism that traps biotin in human milk.
On a molar basis, biotin accounts for approximately half of the total avidin-binding substances in human serum and urine. Biocytin, bisnorbiotin, bisnorbiotin methylketone, biotin sulfoxide, and biotin sulfone form most of the balance. Biotin metabolism is accelerated in some individuals by anticonvulsants and during pregnancy, thereby increasing the ratio of biotin metabolites to biotin excreted in urine.
An alternate fate to being incorporated into carboxylases or unchanged excretion is catabolism to an inactive metabolite before excretion in urine. About half of biotin undergoes metabolism before excretion. Two principal pathways of biotin catabolism have been identified in mammals. In the first pathway, the valeric acid side chain of biotin is degraded by beta oxidation. This leads to the formation of bisnorbiotin, tetranorbiotin, and related intermediates that are known to result from beta-oxidation of fatty acids. The cellular site of this beta-oxidation of biotin is uncertain. Nonenzymatic decarboxylation of the unstable beta-ketobiotin and beta-keto-bisnorbiotin leads to formation of bisnorbiotin methylketone and tetranorbiotin methylketone, which appear in urine. In the second pathway, the sulfur in the thiophane ring of biotin is oxidized, leading to the formation of biotin L-sulfoxide, biotin D-sulfoxide, and biotin sulfone. Combined oxidation of the ring sulfur and beta-oxidation of the side chain lead to metabolites such as bisnorbiotin sulfone. In mammals, degradation of the biotin ring to release carbon dioxide and urea is quantitatively minor.

Toxicity Summary
Biotin is necessary for the proper functioning of enzymes that transport carboxyl units and fix carbon dioxide, and is required for various metabolic functions, including gluconeogenesis, lipogenesis, fatty acid biosynthesis, propionate metabolism, and catabolism of branched-chain amino acids.

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Interactions
Carbamazepine, phenytoin, and phenobarbital can accelerate biotin metabolism and may cause reduced biotin status. Long-term use of carbamazepine, phenytoin, phenobarbital and primidone has been associated with reduced plasma concentrations of biotin.
Antibiotic use may decrease the biotin contribution to the body made by the microflora of the large intestine.
Groups of Holtzman rats were mated and the gravid females were dosed sc with 100 mg D(+)-biotin in 0.2 mL of 0.1 N NaOH/kg body weight on days 0 and 1 of gestation. Nine animals were dosed with biotin only, 7 were given biotin and 0.1 ug 17(beta)-estradiol in 0.05 mL olive oil sc on days 5 to 20 of gestation, and 7 were given biotin and 4 mg progesterone in 0.2 mL olive oil sc on days 5 to 20 of gestation. Nine gravid animals were untreated and used as a negative-control group. Three groups of 6 nongravid animals were dosed in the same manner as the gravid animals and used as nonpregnant treated controls. The animals were killed and examined on day 21 of gestation. Complete resorption of the fetuses occurred in 8 of the 9 rats dosed with biotin only; dosing with estrogen or progesterone prevented the resorptions. Fetal and placental weights from animals dosed with biotin and estrogen or progesterone were decr as compared to controls, but the decr was not statistically significant. Biotin caused a decr in body weights of gravid and nongravid animals; body weights of gravid animals given biotin and progesterone were similar to gravid untreated control, whereas body weights of gravid animals given biotin and estrogen were incr. The uterine weights of gravid animals given biotin and estrogen were similar to that of gravid untreated controls, whereas the uterine weights of animals dosed with biotin and progesterone were statistically significantly decr.
...Groups of Holtzman rats were mated, and gravid females were dosed with 100 mg D(+)-biotin in 0.2 mL of 0.1 N NaOH/kg body weight on days 13 and 14 of gestation. Eleven animals were dosed with biotin only, 7 were given biotin and 0.1 ug 17(beta)-estradiol in 0.05 mL olive oil sc until day 20 of gestation, and 7 were given biotin and 4 mg progesterone in 0.2 mL olive oil sc until day 20 of gestation. Nine gravid animals were untreated and used as a negative-control group. The animals were killed and examined on day 21 of gestation. Resorptions occurred in 2 of the 11 animals dosed with biotin only. The maternal body weights and the fetal, uterine, and placental weights of the remaining 9 animals of this group were statistically significantly decr as compared to controls. The maternal body weights and the fetal, uterine, and placental weights of the animals dosed with biotin and estrogen and the maternal body weights and uterine weights of the animals dosed with biotin and progesterone were similar to control values. Hepatic and ovarian weights were similar for animals of the test and control groups.
For more Interactions (Complete) data for BIOTIN (6 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat oral >1.45 mmol/kg
LD50 Mouse oral >10 g/kg

[1]. Biotin biochemistry and human requirements. J Nutr Biochem, 1999. 10(3): p. 128-38.

[2]. Mock, D.M. Biotin status: which are valid indicators and how do we know? J Nutr, 1999. 129(2S Suppl): p. 498S-503S.

[3]. Biotin. Biofactors. 2009 Jan-Feb;35(1):36-46.

[4]. Biotin uptake by T47D breast cancer cells: functional and molecular evidence of sodium-dependent multivitamin transporter (SMVT). Int J Pharm. 2013 Jan 30;441(1-2):535-43.

[5]. Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes. Free Radic Res. 2019 May;53(5):535-561.

[6]. Biotin amelioration of nephrotoxicity in streptozotocin-induced diabetic mice. Saudi J Biol Sci. 2015 Sep;22(5):564-9.

[7]. Dietary biotin deficiency decreased growth performance and impaired the immune function of the head kidney, spleen and skin in on-growing grass carp (Ctenopharyngodon idella). Fish Shellfish Immunol. 2020 Feb;97:216-234.

Therapeutic Uses
The B vitamins are indicated for prevention and treatment of vitamin B deficiency. Vitamin B deficiency may occur as a result of inadequate nutrition or intestinal malabsorption but does not occur in healthy individuals receiving an adequate balanced diet. Simple nutritional deficiency of individual B vitamins is rare since dietary inadequacy usually results in multiple deficiencies. For prophylaxis of biotin deficiency, dietary improvement, rather than supplementatin, is advisable. For teatment of biotin deficiency, supplementation is preferred. /Included in US product labeling/
Large doses of biotin ... are administered to babies with infantile seborrhea and to individuals with genetic alterations of biotin-dependent enzymes. patients who receive long-term parenteral nutrition should be given vitamin formulations that contain biotin.
(VET): Biotin is used as a feed additive for poultry and swine.
Biotin is used to treat the biotin-responsive inborn errors of metabolism holocarboxylase synthetase deficiency and biotinidase deficiency. Holocarboxylase deficiency is the most common cause of neonatal multiple carboxylase deficiency. Biotinidase deficiency is the most common cause of late-onset multiple carboxylase deficiency.
For more Therapeutic Uses (Complete) data for BIOTIN (11 total), please visit the HSDB record page.

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Drug Warnings
Biotin deficiency, which can occur by the feeding of uncooked egg whites or by the omission of biotin from the diet, can cause alopecia and a characteristic scaly, erythematous dermatitis around body orifices in infants, children, and adults. For adults, prolonged biotin deficiency can result in depression, lethargy, hallucinations, and paresthesias of the extremities.
Biotin has not been proven effective in the treatment of acne, seborrheic eczema, or alopecia.

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Pharmacodynamics
Biotin is a water-soluble B-complex vitamin which is composed of an ureido ring fused with a tetrahydrothiophene ring, which attaches a valeric acid substituent at one of its carbon atoms. Biotin is used in cell growth, the production of fatty acids, metabolism of fats, and amino acids. It plays a role in the Kreb cycle, which is the process in which energy is released from food. Biotin not only assists in various metabolic chemical conversions, but also helps with the transfer of carbon dioxide. Biotin is also helpful in maintaining a steady blood sugar level. Biotin is often recommended for strengthening hair and nails. Consequenty, it is found in many cosmetic and health products for the hair and skin. Biotin deficiency is a rare nutritional disorder caused by a deficiency of biotin. Initial symptoms of biotin deficiency include: Dry skin, Seborrheic dermatitis, Fungal infections, rashes including erythematous periorofacial macular rash, fine and brittle hair, and hair loss or total alopecia. If left untreated, neurological symptoms can develop, including mild depression, which may progress to profound lassitude and, eventually, to somnolence; changes in mental status, generalized muscular pains (myalgias), hyperesthesias and paresthesias. The treatment for biotin deficiency is to simply start taking some biotin supplements. A lack of biotin in infants will lead to a condition called seborrheic dermatitis or "cradle cap". Biotin deficiencies are extremely rare in adults but if it does occur, it will lead to anemia, depression, hair loss, high blood sugar levels, muscle pain, nausea, loss of appetite and inflamed mucous membranes.

C10H16N2O3S

244.3106

244.088

58-85-5

Biotin-d2-1;1217481-41-8;Biotin sodium;56085-82-6;rel-Biotin-d4;1217850-77-5;Biotin-d2

171548

White to off-white solid powder

1.6±0.1 g/cm3

492.3±55.0 °C at 760 mmHg

231-233 °C(lit.)

251.5±31.5 °C

0.0±2.8 mmHg at 25°C

1.717

0.03

103.73

3

4

5

16

298

3

C1[C@H]2[C@@H]([C@@H](S1)CCCCC(=O)O)NC(=O)N2

YBJHBAHKTGYVGT-ZKWXMUAHSA-N

InChI=1S/C10H16N2O3S/c13-8(14)4-2-1-3-7-9-6(5-16-7)11-10(15)12-9/h6-7,9H,1-5H2,(H,13,14)(H2,11,12,15)/t6-,7-,9-/m0/s1

5-[(3aS,4S,6aR)-2-oxo-1,3,3a,4,6,6a-hexahydrothieno[3,4-d]imidazol-4-yl]pentanoic acid

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 (~409.32 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (10.23 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 25.0 mg/mL澄清DMSO储备液加入到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: ≥ 2.5 mg/mL (10.23 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 25.0 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: ≥ 2.5 mg/mL (10.23 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 25.0 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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配方 4 中的溶解度: 1.96 mg/mL (8.02 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶 (<60°C).

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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。