D-Mannose
(Synonyms: D-甘露糖) 目录号 : GC33460
An aldohexose monosaccharide
Cas No.:3458-28-4
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
D-Mannose is an aldohexose monosaccharide and an epimer of glucose. D-Mannose is found in animals, microbes, and plants, can be used as an energy source by conversion to glucose, and can also be produced from glucose.1 It is converted via hexokinase to mannose-6-phosphate and then to intermediates that are incorporated into proteins via N-linked glycosylation. It decreases T cell proliferation and increases FoxP3+ T regulatory cells in vitro and prevents diabetes in non-obese diabetic (NOD) mice, a model of autoimmune diabetes, when administered at a dose of 1.1 M in the drinking water.2 D-Mannose administration during gestation at a dose of 9 mg/ml in the drinking water rescues the embryonic lethal phenotype and prevents deficits in glycosylation in Pmm2R137H/F118L mice, a transgenic model of the congenital glycosylation disorder (CDG) PMM2-CDG, which is characterized by phosphomannomutase 2 (PMM2) gene mutations.3 Levels of D-mannose are reduced in the serum of patients with PMM2-CDG.4 Formulations containing D-mannose have been used in the treatment of mannose phosphate isomerase CDG (MPI-CDG).
1.Sharma, V., Ichikawa, M., and Freeze, H.H.Mannose metabolism: More than meets the eyeBiochim. Biophys. Res. Commun.453(2)220-228(2014) 2.Zhang, D., Chia, C., Jiao, X., et al.D-mannose induces regulatory T cells and suppresses immunopathologyNat. Med.23(9)1036-1045(2017) 3.Schneider, A., Theil, C.R., J., DeRossi, C., et al.Successful prenatal mannose treatment for congenital disorder of glycosylation-Ia in miceNat. Med.18(1)71-73(2011) 4.Panneerselvam, K., Etchison, J.R., Skovby, F., et al.Abnormal metabolism of mannose in families with carbohydrate-deficient glycoprotein syndrome type 1Biochem. Mol. Med.61(2)161-167(1997)
| Cas No. | 3458-28-4 | SDF | |
| 别名 | D-甘露糖 | ||
| Canonical SMILES | OC[C@@H](O)[C@@H](O)[C@H](O)[C@H](O)C=O | ||
| 分子式 | C6H12O6 | 分子量 | 180.16 |
| 溶解度 | Water : ≥ 50 mg/mL (277.53 mM);DMSO : 50 mg/mL (277.53 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 5.5506 mL | 27.7531 mL | 55.5062 mL |
| 5 mM | 1.1101 mL | 5.5506 mL | 11.1012 mL |
| 10 mM | 0.5551 mL | 2.7753 mL | 5.5506 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
D-Mannose suppresses macrophage IL-1β production
Nat Commun 2020 Dec 11;11(1):6343.PMID:33311467DOI:10.1038/s41467-020-20164-6.
D-Mannose is a monosaccharide approximately a hundred times less abundant than glucose in human blood. Previous studies demonstrated that supraphysiological levels of D-Mannose inhibit tumour growth and stimulate regulatory T cell differentiation. It is not known whether D-Mannose metabolism affects the function of non-proliferative cells, such as inflammatory macrophages. Here, we show that D-Mannose suppresses LPS-induced macrophage activation by impairing IL-1β production. In vivo, mannose administration improves survival in a mouse model of LPS-induced endotoxemia as well as decreases progression in a mouse model of DSS-induced colitis. Phosphomannose isomerase controls response of LPS-activated macrophages to D-Mannose, which impairs glucose metabolism by raising intracellular mannose-6-phosphate levels. Such alterations result in the suppression of succinate-mediated HIF-1α activation, imposing a consequent reduction of LPS-induced Il1b expression. Disclosing an unrecognized metabolic hijack of macrophage activation, our study points towards safe D-Mannose utilization as an effective intervention against inflammatory conditions.
D-Mannose vs other agents for recurrent urinary tract infection prevention in adult women: a systematic review and meta-analysis
Am J Obstet Gynecol 2020 Aug;223(2):265.e1-265.e13.PMID:32497610DOI:10.1016/j.ajog.2020.05.048.
Objective: We performed a systematic review and meta-analysis to determine whether D-Mannose reduces urinary tract infection recurrence (ie, cumulative incidence) in adult women with recurrent urinary tract infection compared with other prevention agents. Secondary outcomes included side effects and compliance with D-Mannose use. Data sources: Ovid Medline 1946-, Embase 1947-, Scopus 1823-, Cochrane Library, Web of Science 1900-, and ClinicalTrials.gov were searched through 4/15/2020. Study eligibility criteria: Systematic review inclusion: randomized controlled trials, prospective cohorts, and retrospective cohorts written in English of women ≥18 years old with recurrent urinary tract infection in which D-Mannose was utilized as an outpatient prevention regimen. Systematic review exclusion: lab or animal-based research, study protocols only, and conference abstracts. Meta-analysis inclusion: stated D-Mannose dose, follow-up time ≥6 months, a comparison arm to D-Mannose, and data available from women ≥18 years of age. Study appraisal and synthesis methods: Two independent reviewers made abstract, full text, and data extraction decisions. Study methodologic quality was assessed using the Cochrane Risk of Bias tool. Relative risks, confidence intervals, and heterogeneity were computed. Results: Searches identified 776 unique citations. Eight publications met eligibility: 2 using D-Mannose only; 6 using D-Mannose combined with another treatment. Seven studies were prospective: 2 randomized controlled trials, 1 randomized cross-over trial, and 4 prospective cohort studies. One retrospective cohort study was included. Three studies met meta-analysis eligibility (1 randomized controlled trial, 1 randomized cross-over trial, and 1 prospective cohort). Pooled relative risk of urinary tract infection recurrence comparing D-Mannose to placebo was 0.23 (95% confidence interval, 0.14-0.37; heterogeneity=0%; D-Mannose n=125, placebo n=123). Pooled relative risk of urinary tract infection recurrence comparing D-Mannose to preventative antibiotics was 0.39 (95% confidence interval, 0.12-1.25; heterogeneity=88%; D-Mannose n=163, antibiotics n=163). Adverse side effects were reported in 2 studies assessing D-Mannose only (1 study (n=10) reported none; the other reported a low incidence (8/103 participants) of diarrhea). Two studies reported compliance, which was high. Conclusion: D-Mannose appears protective for recurrent urinary tract infection (vs placebo) with possibly similar effectiveness as antibiotics. Overall, D-Mannose appears well tolerated with minimal side effects-only a small percentage experiencing diarrhea. Meta-analysis interpretation must consider the small number of studies with varied study design and quality and the overall small sample size.
D-Mannose facilitates immunotherapy and radiotherapy of triple-negative breast cancer via degradation of PD-L1
Proc Natl Acad Sci U S A 2022 Feb 22;119(8):e2114851119.PMID:35181605DOI:10.1073/pnas.2114851119.
Breast cancer is the most frequent malignancy in women worldwide, and triple-negative breast cancer (TNBC) patients have the worst prognosis and highest risk of recurrence. The therapeutic strategies for TNBC are limited. It is urgent to develop new methods to enhance the efficacy of TNBC treatment. Previous studies demonstrated that D-Mannose, a hexose, can enhance chemotherapy in cancer and suppress the immunopathology of autoimmune diseases. Here, we show that D-Mannose can significantly facilitate TNBC treatment via degradation of PD-L1. Specifically, D-Mannose can activate AMP-activated protein kinase (AMPK) to phosphorylate PD-L1 at S195, which leads to abnormal glycosylation and proteasomal degradation of PD-L1. D-mannose-mediated PD-L1 degradation promotes T cell activation and T cell killing of tumor cells. The combination of D-Mannose and PD-1 blockade therapy dramatically inhibits TNBC growth and extends the lifespan of tumor-bearing mice. Moreover, D-mannose-induced PD-L1 degradation also results in messenger RNA destabilization of DNA damage repair-related genes, thereby sensitizing breast cancer cells to ionizing radiation (IR) treatment and facilitating radiotherapy of TNBC in mice. Of note, the effective level of D-Mannose can be easily achieved by oral administration in mice. Our study unveils a mechanism by which D-Mannose targets PD-L1 for degradation and provides methods to facilitate immunotherapy and radiotherapy in TNBC. This function of D-Mannose may be useful for clinical treatment of TNBC.
Role of D-Mannose in the Prevention of Recurrent Urinary Tract Infections: Evidence from a Systematic Review of the Literature
Eur Urol Focus 2021 Sep;7(5):1166-1169.PMID:32972899DOI:10.1016/j.euf.2020.09.004.
The inexorable rise of antimicrobial resistance reinforces the need for alternative approaches to both treat and prevent urinary tract infections (UTIs). A potential approach is administration of D-Mannose, an inert monosaccharide that is metabolised and excreted in urine and acts by inhibiting bacterial adhesion to the urothelium. We performed a systematic review to assess the effect of D-Mannose in the prevention of recurrent UTIs. Of the eight studies reporting on D-Mannose in this context, six were clinical and included 695 individuals. Three studies reported that time to UTI recurrence was longer with D-Mannose. D-Mannose improved quality of life and significantly reduced recurrent UTIs in both catheter and non-catheter users. D-Mannose was effective in reducing the incidence of recurrent UTIs and prolonging UTI-free periods, which consequently increased quality of life. PATIENT SUMMARY: D-Mannose is a sugar that seems to reduce the incidence of recurrent urinary tract infections and associated bothersome symptoms. It also leads to a longer duration between episodes of recurrences and consequently improves patient quality of life. D-Mannose can be used as a supplementary or alternate treatment for recurrent urinary tract infections.
D-Mannose alleviates osteoarthritis progression by inhibiting chondrocyte ferroptosis in a HIF-2α-dependent manner
Cell Prolif 2021 Nov;54(11):e13134.PMID:34561933DOI:10.1111/cpr.13134.
Objectives: Chondrocyte ferroptosis contributes to osteoarthritis (OA) progression, and D-Mannose shows therapeutic value in many inflammatory conditions. Here, we investigated whether D-Mannose interferes in chondrocyte ferroptotic cell death during osteoarthritic cartilage degeneration. Materials and methods: In vivo anterior cruciate ligament transection (ACLT)-induced OA mouse model and an in vitro study of chondrocytes in an OA microenvironment induced by interleukin-1β (IL-1β) exposure were employed. Combined with Epas1 gene gain- and loss-of-function, histology, immunofluorescence, quantitative RT-PCR, Western blot, cell viability and flow cytometry experiments were performed to evaluate the chondroprotective effects of D-Mannose in OA progression and the role of hypoxia-inducible factor 2 alpha (HIF-2 α) in D-mannose-induced ferroptosis resistance of chondrocytes. Results: D-Mannose exerted a chondroprotective effect by attenuating the sensitivity of chondrocytes to ferroptosis and alleviated OA progression. HIF-2α was identified as a central mediator in D-mannose-induced ferroptosis resistance of chondrocytes. Furthermore, overexpression of HIF-2α in chondrocytes by Ad-Epas1 intra-articular injection abolished the chondroprotective effect of D-Mannose during OA progression and eliminated the role of D-Mannose as a ferroptosis suppressor. Conclusions: D-Mannose alleviates osteoarthritis progression by suppressing HIF-2α-mediated chondrocyte sensitivity to ferroptosis, indicating D-Mannose to be a potential therapeutic strategy for ferroptosis-related diseases.