Indole-3-carboxaldehyde
(Synonyms: 吲哚-3-甲醛; 3-吲哚甲醛; 3-Formylindole) 目录号 : GC38918
An active tryptophan metabolite and synthetic intermediate
Cas No.:487-89-8
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: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Indole-3-carboxyaldehyde is an active metabolite of tryptophan and a synthetic intermediate.1,2,3 It is produced by lactobacilli in the gut microbiota via the indole pyruvate pathway, which is catalyzed by aromatic amino acid aminotransferase (ArAT).1 Indole-3-carboxyaldehyde (18 mg/kg) increases colonic production of IL-22 and restores colonization resistance to C. albicans infection in a wild-type, but not aryl hydrocarbon receptor knockout (Ahr-/-), mouse model of mucosal candidiasis. It also reduces intestinal mucosal damage in a mouse model of colitis induced by dextran sulfate . Indole-3-carboxaldehyde has been used as a synthetic intermediate in the synthesis of Schiff bases and ergot alkaloids.2,3
1.Zelante, T., Iannitti, R.G., Cunha, C., et al.Tryptophan catabolites from microbiota engage aryl hydrocarbon receptor and balance mucosal reactivity via interleukin-22Immunity39(2)372-385(2013) 2.Sinha, D., Tiwari, A.K., Singh, S., et al.Synthesis, characterization and biological activity of Schiff base analogues of indole-3-carboxaldehydeEur. J. Med. Chem.43(1)160-165(2008) 3.Somei, M.Studies directed toward the ultimate synthesis for ergot alkaloidsYakugaku Zasshi108(5)361-380(1988)
| Cas No. | 487-89-8 | SDF | |
| 别名 | 吲哚-3-甲醛; 3-吲哚甲醛; 3-Formylindole | ||
| Canonical SMILES | O=CC1=CNC2=C1C=CC=C2 | ||
| 分子式 | C9H7NO | 分子量 | 145.16 |
| 溶解度 | DMSO: 20 mg/mL (137.78 mM); Methanol: < 1 mg/mL (insoluble); Water: < 0.1 mg/mL (insoluble) | 储存条件 | Store at RT |
| 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 | 6.889 mL | 34.4448 mL | 68.8895 mL |
| 5 mM | 1.3778 mL | 6.889 mL | 13.7779 mL |
| 10 mM | 0.6889 mL | 3.4445 mL | 6.889 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。
Plant-Derived Exosomal MicroRNAs Shape the Gut Microbiota
Cell Host Microbe 2018 Nov 14;24(5):637-652.e8.PMID:30449315DOI:10.1016/j.chom.2018.10.001.
The gut microbiota can be altered by dietary interventions to prevent and treat various diseases. However, the mechanisms by which food products modulate commensals remain largely unknown. We demonstrate that plant-derived exosome-like nanoparticles (ELNs) are taken up by the gut microbiota and contain RNAs that alter microbiome composition and host physiology. Ginger ELNs (GELNs) are preferentially taken up by Lactobacillaceae in a GELN lipid-dependent manner and contain microRNAs that target various genes in Lactobacillus rhamnosus (LGG). Among these, GELN mdo-miR7267-3p-mediated targeting of the LGG monooxygenase ycnE yields increased Indole-3-carboxaldehyde (I3A). GELN-RNAs or I3A, a ligand for aryl hydrocarbon receptor, are sufficient to induce production of IL-22, which is linked to barrier function improvement. These functions of GELN-RNAs can ameliorate mouse colitis via IL-22-dependent mechanisms. These findings reveal how plant products and their effects on the microbiome may be used to target specific host processes to alleviate disease.
Indole-3-carboxaldehyde regulates RSV-induced inflammatory response in RAW264.7 cells by moderate inhibition of the TLR7 signaling pathway
J Nat Med 2021 Jun;75(3):602-611.PMID:33755912DOI:10.1007/s11418-021-01506-0.
Human respiratory syncytial virus (RSV) is highly contagious and the leading cause of severe respiratory tract illness in infants, elderly, and immunocompromised individuals. Toll-like receptor 7 (TLR7), a pattern recognition receptor recognising the ssRNA of RSV, activates proinflammatory pathways and triggers secretion of interferons (IFNs). On the one hand, the inflammatory responses help clear out virus. On the other hand, they lead to severe lung damage. Banlangen is a traditional Chinese herbal medicine commonly prescribed for respiratory virus infection treatment, but the mechanisms of action and active components remain largely unknown. In the present study, we investigated the effects of the main active components of total alkaloids from banlangen (epigoitrin, Indole-3-carboxaldehyde, indole-3-acetonitrile and 4-methoxyindole-3-acetonitrile) on the RSV-induced inflammatory responses in mouse macrophage cells (RAW264.7). Our results demonstrated that RSV-induced IFN-α excessive secretion was moderately inhibited by Indole-3-carboxaldehyde through downregulation of mRNA expression in a dose-dependent manner, in comparison, the inhibitory effects of ribavirin were too strong. Furthermore, we revealed that Indole-3-carboxaldehyde suppressed transcription of IFN-α by inhibiting RSV-induced TLR7 expression in RAW264.7 cells. Additionally, Indole-3-carboxaldehyde inhibited RSV-induced NF-κB signalling activation in a TLR7-MyD88-dependent manner. Together, our findings suggest that Indole-3-carboxaldehyde inhibited RSV-induced inflammatory injury by moderate regulation of TLR7 signaling pathway and did not significantly affect the viral clearance competence of the innate immune system.
Indole-3-carboxaldehyde Restores Gut Mucosal Integrity and Protects from Liver Fibrosis in Murine Sclerosing Cholangitis
Cells 2021 Jun 29;10(7):1622.PMID:34209524DOI:10.3390/cells10071622.
Primary sclerosing cholangitis (PSC) is a long-term liver disease characterized by a progressive course of cholestasis with liver inflammation and fibrosis. Intestinal barrier dysfunction has been implicated in the pathogenesis of PSC. According to the "leaky gut" hypothesis, gut inflammation alters the permeability of the intestinal mucosa, with the translocation of gut-derived products that enter the enterohepatic circulation and cause hepatic inflammation. Thus, the administration of molecules that preserve epithelial barrier integrity would represent a promising therapeutic strategy. Indole-3-carboxaldehyde (3-IAld) is a microbial-derived product working at the interface between the host and the microbiota and is able to promote mucosal immune homeostasis in a variety of preclinical settings. Herein, by resorting to a murine model of PSC, we found that 3-IAld formulated for localized delivery in the gut alleviates hepatic inflammation and fibrosis by modulating the intestinal microbiota and activating the aryl hydrocarbon receptor-IL-22 axis to restore mucosal integrity. This study points to the therapeutic potential of 3-IAld in liver pathology.
Enteric formulated Indole-3-carboxaldehyde targets the aryl hydrocarbon receptor for protection in a murine model of metabolic syndrome
Int J Pharm 2021 Jun 1;602:120610.PMID:33865951DOI:10.1016/j.ijpharm.2021.120610.
The metabolic syndrome (MetSyn) is a disorder characterized by a cluster of diseases where the regulation of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor endowed with ligand- and context-dependent activities, can have a major therapeutic relevance. We have recently discovered a tryptophan metabolite of microbial origin, Indole-3-carboxaldehyde (3-IAld), able to regulate intestinal mucosal homeostasis by acting as a ligand of AhR. This makes 3-IAld a potential candidate to treat MetSyn related ailments. Herein, we provide a proof of concept on the efficacy and safety of 3-IAld encapsulated in enteric microparticles (MP) in vivo in a MetSyn murine model. In particular, we showed that 3-IAld: i) is released from MPs in the intestine and potentially metabolized; ii) is able to activate AhR locally; iii) prevents the metabolic complications and the intestinal epithelial barrier dysfunction; iv) is not associated with toxic events. This study does not only extend the biological activity of 3-IAld in vivo, but also provides hints on the therapeutic potential of 3-IAld delivered by enteric MP in MetSyn related diseases.
Optimizing therapeutic outcomes of immune checkpoint blockade by a microbial tryptophan metabolite
J Immunother Cancer 2022 Mar;10(3):e003725.PMID:35236743DOI:10.1136/jitc-2021-003725.
Background: Despite the great success, the therapeutic benefits of immune checkpoint inhibitors (ICIs) in cancer immunotherapy are limited by either various resistance mechanisms or ICI-associated toxic effects including gastrointestinal toxicity. Thus, novel therapeutic strategies that provide manageable side effects to existing ICIs would enhance and expand their therapeutic efficacy and application. Due to its proven role in cancer development and immune regulation, gut microbiome has gained increasing expectation as a potential armamentarium to optimize immunotherapy with ICI. However, much has to be learned to fully harness gut microbiome for clinical applicability. Here we have assessed whether microbial metabolites working at the interface between microbes and the host immune system may optimize ICI therapy. Methods: To this purpose, we have tested Indole-3-carboxaldehyde (3-IAld), a microbial tryptophan catabolite known to contribute to epithelial barrier function and immune homeostasis in the gut via the aryl hydrocarbon receptor (AhR), in different murine models of ICI-induced colitis. Epithelial barrier integrity, inflammation and changes in gut microbiome composition and function were analyzed. AhR, indoleamine 2,3-dioxygenase 1, interleukin (IL)-10 and IL-22 knockout mice were used to investigate the mechanism of 3-IAld activity. The function of the microbiome changes induced by 3-IAld was evaluated on fecal microbiome transplantation (FMT). Finally, murine tumor models were used to assess the effect of 3-IAld treatment on the antitumor activity of ICI. Results: On administration to mice with ICI-induced colitis, 3-IAld protected mice from intestinal damage via a dual action on both the host and the microbes. Indeed, paralleling the activation of the host AhR/IL-22-dependent pathway, 3-IAld also affected the composition and function of the microbiota such that FMT from 3-IAld-treated mice protected against ICI-induced colitis with the contribution of butyrate-producing bacteria. Importantly, while preventing intestinal damage, 3-IAld did not impair the antitumor activity of ICI. Conclusions: This study provides a proof-of-concept demonstration that moving past bacterial phylogeny and focusing on bacterial metabolome may lead to a new class of discrete molecules, and that working at the interface between microbes and the host immune system may optimize ICI therapy.