Product Name Genipin
CAS No.: 6902-77-8
Catalog No.: CFN99142
Molecular Formula: C11H14O5
Molecular Weight: 226.23 g/mol
Purity: >=98%
Type of Compound: Iridoids
Physical Desc.: White powder
Targets: ERK | TNF-α | MMP(e.g.TIMP) | JNK | AMPK | VEGFR | Phospholipase (e.g. PLA) | COX | NF-kB | PI3K | Akt | ROS | MAPK | AP-1
Source: The fruits of Gardenia jasminoides Ellis
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $40/20mg
Genipin is an excellent natural cross-linker for proteins, collagen, gelatin, and chitosan cross-linking, can be used as a regulating agent for drug delivery, as the raw material for gardenia blue pigment preparation. It is a novel chemical activator of EBV lytic cycle and a cell permeable inhibitor of uncoupling protein 2 (UCP2). Genipin has antimicrobial,antiviral, antitumor, and anti-inflammatory effects, it is used for choleretic action for liver diseases control and could be used for the treatment of periodontal disease to prevent MMPs expression in periodontal lesion. It shows an antithrombotic effect in vivo due to the suppression of platelet aggregation.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to:

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    J Microbiol. 2015 Feb;53(2):155-65.
    Genipin as a novel chemical activator of EBV lytic cycle.[Pubmed: 25626372]
    Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus that causes acute infection and establishes life-long latency. EBV causes several human cancers, including Burkitt's lymphoma, nasopharyngeal and gastric carcinoma. Antiviral agents can be categorized as virucides, antiviral chemotherapeutic agents, and immunomodulators. Most antiviral agents affect actively replicating viruses, but not their latent forms. Novel antiviral agents must be active on both the replicating and the latent forms of the virus. Gardenia jasminoides is an evergreen flowering plant belonging to the Rubiaceae family and is most commonly found growing wild in Vietnam, Southern China, Taiwan, Japan, Myanmar, and India. Genipin is an aglycone derived from an iridoid glycoside called geniposide, which is present in large quantities in the fruit of G. jasminoides.
    In this study, Genipin was evaluated for its role as an antitumor and antiviral agent that produces inhibitory effects against EBV and EBV associated gastric carcinoma (EBVaGC). In SNU719 cells, one of EBVaGCs, Genipin caused significant cytotoxicity (70 μM), induced methylation on EBV C promoter and tumor suppressor gene BCL7A, arrested cell-cycle progress (S phases), upregulated EBV latent/lytic genes in a dose-dependent manner, stimulated EBV progeny production, activated EBV F promoter for EBV lytic activation, and suppressed EBV infection.
    These results indicated that Genipin could be a promising candidate for antiviral and antitumor agents against EBV and EBVaGC.
    Biomaterials. 2013 Oct;34(31):7754-65.
    Induction of angiogenesis using VEGF releasing genipin-crosslinked electrospun gelatin mats.[Pubmed: 23863451]
    Rapid and controlled vascularization of engineered tissues remains one of the key limitations in tissue engineering applications.
    This study investigates the possible use of natural extracellular matrix-like scaffolds made of gelatin loaded with human vascular endothelial growth factor (VEGF), as a bioresorbable platform for long-term release and consequent angiogenic boosting. For this aim, gelatin was firstly electrospun and then cross-linked at two different concentrations (0.1% and 0.5% w/v) by using Genipin, a low toxic agent, in order to fabricate a suitable substrate to be loaded with VEGF. Collected fibers were homogeneous and free of beads, the fibrous structure was retained after cross-linking. Mechanical properties were deeply affected by the chemical treatment showing a different behavior, depending on the testing conditions (i.e., dry or wet state). VEGF release was assessed by means of ELISA assay: a cumulative release of about 90% (0.1% w/v) and 60% (0.5% w/v) at 28 days was measured. Both VEGF loaded mats induced cell viability, endothelial differentiation and showed chemoattractive properties when tested on human mesenchymal stromal cells (hMSCs). In vitro and in vivo angiogenic assays demonstrated that the VEGF loaded mats induced an angiogenic potential in stimulating new vessel formation similar, if not superior, to fresh VEGF. VEGF retains bioactive and pro-angiogenic potential for up to 14 days.
    The results demonstrated that Genipin cross-linked electrospun gelatin mats loaded with VEGF could be part of a useful strategy to stimulate and induce angiogenesis in tissue engineered applications.
    Biochimie. 2014 Dec;107 Pt B:391-5.
    Genipin inhibits MMP-1 and MMP-3 release from TNF-a-stimulated human periodontal ligament cells.[Pubmed: 25457105]
    Genipin, the aglycon of geniposide found in gardenia fruit has long been considered for treatment of inflammatory diseases in traditional oriental medicine. Genipin has recently been reported to have some pharmacological functions, such as antimicrobial, antitumor, and anti-inflammatory effects.
    The aim of this study was to examine whether Genipin could modify matrix metalloproteinase (MMP)-1 and MMP-3, which are related to the destruction of periodontal tissues in periodontal lesion, expression in tumor necrosis factor (TNF)-α-stimulated human periodontal ligament cells (HPDLCs). Genipin prevented TNF-α-mediated MMP-1 and MMP-3 productions in HPDLCs. Moreover, Genipin could suppress not only extracellular signal-regulated kinase (ERK) and Jun-N-terminal kinase (JNK) phosphorylations but also AMP-activated protein kinase (AMPK) phosphorylation in TNF-α-stimulated HPDLCs. Inhibitors of ERK and AMPK could inhibit both MMP-1 and MMP-3 productions. Moreover, we revealed the ERK inhibitor suppressed AMPK phosphorylation in TNF-α-stimulated HPDLCs.
    These data provide a new mechanism through which Genipin could be used for the treatment of periodontal disease to prevent MMPs expression in periodontal lesion.
    Food Chem Toxicol. 2014 Feb;64:126-34.
    Genipin induces cyclooxygenase-2 expression via NADPH oxidase, MAPKs, AP-1, and NF-κB in RAW 264.7 cells.[Pubmed: 24296130 ]
    Genipin is a compound found in gardenia fruit extract with diverse pharmacological activities. However, the mechanism underlying Genipin-induced cyclooxygenase-2 (COX-2) expression remains unknown.
    In this study, we investigated the effects of Genipin on COX-2 expression and determined that exposure to Genipin dose-dependently enhanced the production of prostaglandin E2 (PGE2), a major COX-2 metabolite, in RAW 264.7 cells. These effects were mediated by Genipin-induced activation of the COX-2 promoter, as well as AP-1 and NF-κB luciferase constructs. Phosphatidylinositol-3-kinase/Akt and MAPKs were also significantly activated by Genipin, and Akt and MAPKs inhibitors (PD98059, SB20358, SP600125, and LY294002) inhibited Genipin-induced COX-2 expression. Moreover, Genipin increased production of the ROS and the ROS-producing NAPDH-oxidase (NOX) family oxidases, NOX2 and NOX3. Inhibition of NADPH with diphenyleneiodonium attenuated ROS production, COX-2 expression and NF-κB and AP-1 activation.
    These results suggest that the molecular mechanism mediating ROS-dependent COX-2 up-regulation and PGE2 production by Genipin involves activation of Akt, MAPKs and AP-1/NF-κB.
    Cell Metab. 2006 Jun;3(6):417-27.
    Genipin inhibits UCP2-mediated proton leak and acutely reverses obesity- and high glucose-induced beta cell dysfunction in isolated pancreatic islets.[Pubmed: 16753577 ]
    Uncoupling protein 2 (UCP2) negatively regulates insulin secretion. UCP2 deficiency (by means of gene knockout) improves obesity- and high glucose-induced beta cell dysfunction and consequently improves type 2 diabetes in mice.
    In the present study, we have discovered that the small molecule, Genipin, rapidly inhibits UCP2-mediated proton leak. In isolated mitochondria, Genipin inhibits UCP2-mediated proton leak. In pancreatic islet cells, Genipin increases mitochondrial membrane potential, increases ATP levels, closes K(ATP) channels, and stimulates insulin secretion. These actions of Genipin occur in a UCP2-dependent manner. Importantly, acute addition of Genipin to isolated islets reverses high glucose- and obesity-induced beta cell dysfunction.
    Thus, Genipin and/or chemically modified variants of Genipin are useful research tools for studying biological processes thought to be controlled by UCP2. In addition, these agents represent lead compounds that comprise a starting point for the development of therapies aimed at treating beta cell dysfunction.
    Planta Med. 2001 Dec;67(9):807-10.
    Antithrombotic effect of geniposide and genipin in the mouse thrombosis model.[Pubmed: 11745015 ]
    Rapid and controlled vascularization of engineered tissues remains one of the key limitations in tissue engineering applications.
    Geniposide is one of the constituents of Gardenia fruit (Gardenia jasminoides Ellis, Rubiaceae), which has been used in traditional medicine. Although its anti-inflammatory and antithrombotic effects have been reported, the way it acts is still unclear.
    We have investigated the effects of geniposide and its metabolite Genipin on thrombogenesis and platelet aggregation. In an in vivo model, geniposide and Genipin significantly (P < 0.05) prolonged the time required for thrombotic occlusion induced by photochemical reaction in the mouse femoral artery. In an in vitro study, both geniposide and Genipin inhibited collagen-induced, but did not inhibit arachidonate-induced, mouse platelet aggregation. However aspirin, a cyclooxygenase inhibitor, inhibited arachidonate-induced platelet aggregation but only partially inhibited the collagen-induced one. We also showed, by measuring PLA(2)-catalyzed arachidonic acid release, that geniposide inhibited phospholipase A(2) (PLA(2)) activity.
    We conclude that geniposide showed an antithrombotic effect in vivo due to the suppression of platelet aggregation. PLA(2) inhibition by geniposide is one possible anti-platelet mechanism.

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