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  • Brand : BIOFRON

  • Catalogue Number : BF-M3012

  • Specification : 98%

  • CAS number : 90-33-5

  • Formula : C10H8O3

  • Molecular Weight : 176.17

  • PUBCHEM ID : 5280567

  • Volume : 100mg

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Catalogue Number


Analysis Method






Molecular Weight



White needle crystal

Botanical Source

Eucommia ulmoides

Structure Type



Standards;Natural Pytochemical;API




LM 94/7-hydroxy-4-methyl-coumarin/BMU/CantabbY/Medilla/7-hydroxy-4-methyl-chromen-2-one/4-Methylumbelliferone/Crodimon/4-methyl-7-hydroxy coumarin/Bilcolic/Himecol/7-hydroxy-4-methyl-2H-chromen-2-one/Eurogale/7-Hydroxy-4-methylcoumarin




1.319 g/cm3


Methanol; DMSO

Flash Point


Boiling Point

377.4ºC at 760 mmHg

Melting Point

188.5-190 °C(lit.)


InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:90-33-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Depletion of the cartilage proteoglycan aggrecan is one of the earliest events that occurs in association with osteoarthritis. This loss is often accompanied by a coordinate loss in another glycosaminoglycan, hyaluronan. Chondrocytes experimentally depleted of cell-associated hyaluronan respond by switching to a pro-catabolic metabolism that includes enhanced production of endogenous inflammatory mediators and increased synthesis of matrix metalloproteinases. Hyaluronan turnover is also increased. Together, such a response provides for possible establishment of a self-perpetuating spiral of events that maintains or prolongs the pro-catabolic state. Chondrocytes or cartilage can also be activated by treatment with pro-inflammatory cytokines and mediators such as IL-1β, TNFα, LPS, fibronectin fragments, and hyaluronan oligosaccharides. To determine the mechanism of chondrocyte activation due to hyaluronan loss, a depletion method was required that did not include degrading the hyaluronan. In recent years, several laboratories have used the coumarin derivative, 4-methylumbelliferone, as a potent inhibitor of hyaluronan biosynthesis, due in part to its ability to sequester intracellular UDP-glucuronic acid and inhibition of hyaluronan synthase transcription. However, contrary to our expectation, although 4-methylumbelliferone was indeed an inhibitor of hyaluronan biosynthesis, this depletion did not give rise to an activation of chondrocytes or cartilage. Rather, 4-methylumbelliferone directly and selectively blocked gene products associated with the pro-catabolic metabolic state of chondrocytes and did so through a mechanism preceding and independent of hyaluronan inhibition. These data suggest that 4-methylumbelliferone has additional useful applications to block pro-inflammatory cell activation events but complicates how it is used for defining functions related to hyaluronan.

© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.


4-methylumbelliferone; cartilage biology; chondrocyte; hyaluronan; matrix metalloproteinase (MMP); osteoarthritis


4-Methylumbelliferone Diminishes Catabolically Activated Articular Chondrocytes and Cartilage Explants via a Mechanism Independent of Hyaluronan Inhibition.


Ishizuka S1, Askew EB1, Ishizuka N1, Knudson CB1, Knudson W2.

Publish date

2016 Jun 3




The inflammatory response is closely associated with cancer cell survival. It has been reported that inflammatory signaling cascades promote tumor survival and exert detrimental effects in normal tissue. Hyaluronans have different cellular functions depending on their molecular weights and high molecular weight-hyaluronan (HMW-HA) exhibits anti-inflammatory effects. A previous study determined that the co-administration of 4-methylumbelliferone (4-MU) and X-ray irradiation enhanced anti-tumor and anti-inflammatory effects in HT1080 human fibrosarcoma cells. However, many mechanisms underlie the effect of hyaluronan molecular weight on cells and the induction of anti-inflammatory effects via 4-MU. The present study aimed to determine the relationship between hyaluronan synthesis inhibition by 4-MU and its anti-inflammatory and radio-sensitizing effect in the context of hyaluronan molecular weight. The hyaluronan concentration following 2 Gy X-ray irradiation and/or 4-MU administration was analyzed via ELISA. Additionally, the mRNA expressions of hyaluronan synthase (HAS) by 4-MU and various inflammatory cytokines and interleukins (IL) following exogenous HMW-HA administration were evaluated via Reverse transcription-quantitative PCR. Invasive potential was assessed by matrigel transwell assays and cell survival following exposure to 4-MU with HMW-HA was determined using a clonogenic potency assay. The results of the present study demonstrated that 4-MU suppressed HMW-HA production by inhibiting HAS2 and HAS3 expression. In addition, the surviving fraction of fibrosarcoma cells were rescued from the cell-killing effect of 4-MU via the exogenous administration of HMW-HA. The mRNA levels of certain inflammatory cytokines, including IL-1α, IL-36γ and IL-37 were elevated following HMW-HA administration. The surviving fraction of cells irradiated with 2 Gy alone did not increase following exogenous HMW-HA administration. The results of the present study indicated that the radio-sensitizing effect of 4-MU and the inhibitory effect on hyaluronan synthesis were not closely associated. It was also revealed that IL-1α, IL-36γ and IL-37 were associated with the cell-killing effect of 4-MU in HT1080 cells.

Copyright: © Hasegawa et al.


4-methylumbelliferone; hyaluronan; inflammatory cytokine; interleukin


4-methylumbelliferone inhibits clonogenic potency by suppressing high molecular weight-hyaluronan in fibrosarcoma cells.


Hasegawa K1, Saga R1, Takahashi R1, Fukui R1, Chiba M2, Okumura K3, Tsuruga E1, Hosokawa Y1.

Publish date

2020 Apr




In Graves’ orbitopathy (GO), hyaluronan secreted by orbital fibroblasts contributes to orbital tissue expansion. The goal of this research was to evaluate the potential benefit of 4-methylumbelliferone (4-MU), a hyaluronan synthase (HAS) inhibitor, in primary cultured orbital fibroblasts from Graves’ orbitopathy.

We assessed the viability of orbital fibroblasts using a live/dead cell assay. Hyaluronan synthesis was evaluated by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time PCR (qPCR). Adipogenesis was assessed by Oil Red O staining and qPCR of adipogenic transcription factors.

In orbital fibroblasts treated with 4-MU (up to 1000 μM), cell viability was preserved by 90%. 4-MU significantly inhibited HAS gene expression and hyaluronan production (*P < 0.05). With respect to adipogenesis, 4-MU suppressed the accumulation of lipids and reduced the number of adipocytes, while decreasing expression of adipogenic transcription factors.

4-MU represents a promising new therapeutic agent for GO based on its ability to inhibit hyaluronan production and adipogenesis, without decreasing cell viability.


4-methylumbelliferone; Adipogenesis; Graves’ orbitopathy; Hyaluronic acid


4-Methylumbelliferone suppresses hyaluronan and adipogenesis in primary cultured orbital fibroblasts from Graves' orbitopathy.


Yoon Y1, Chae MK2, Lee EJ3, Yoon JS4.

Publish date

2020 May

Description :

4-Methylumbelliferone is a hyaluronic acid biosynthesis inhibitor with antitumoral and antimetastatic effects.