CeruLenin inhibits the production of catalysts and sterols in dyes by covalently binding to the catalytic site of FAS and interfering with the condensation process between acetone-CoA and propylene glycol-CoA. The MICs of the ABC transgenic mutant strain (ΔTruMDR2) were 1.9 μg/mL and 63 μg/mL, respectively, while the MICs of the wild-type strain (MYA3108) were 125 and 7.5 μg/mL. MIC values for CeruLenin and fluconazole controls. The mutant strain's MICs were 30 and 15 μg/mL, while the wild-type strain's MICs were 63 and 125 μg/mL, respectively [1]. Pretreatment of the model of endothelial dysfunction with the plant synthetase and HMG-CoA reductase inhibitors CeruLenin (5 μg/mL) and lovastatin preceded palmitic acid administration in order to investigate the mechanisms behind the protective benefits of obesogenic quickly regulated protein (StAR). (Lovastatin). Following addition, NO generation was increased and the mRNA expression of TNFα, IL-6, VCAM-1, and IL-1β decreased [2].

The body weight of ob/ob mice is significantly affected by CeruLenin therapy. The treated mice's body weight dropped after two days of treatment, whereas the simulated body weight rose by 5.7%. No weight reduction was seen with the prolonged (7-day) therapy, however weight gain was reduced. When it came to preventing weight gain, CeruLenin at 60 mg/kg worked better than 30 mg/kg in every group. Following a 7-day course of therapy with 60 mg/kg CeruLenin, the ATP content of the daily and every other-day formulations increased by 58.1% and 61.5%, respectively. Additionally, after just two days of therapy with 60 mg/kg CeruLenin, a significant increase in ATP was seen. In contrast, there was no discernible change in the amount of cellular ATP after two or seven days of treatment of 30 mg/kg CeruLenin [3].

Toxicity Summary
This product irreversibly binds to fatty acid synthases, particularly β-ketoacyl-acyl carrier protein synthases (FabH, FabB, and FabF condensates). Significant upregulation of fatty acid synthase (FAS) expression and activity has been observed in various tumor cells and cell lines. Cerulenin inhibition of FAS leads to cytotoxicity and apoptosis in human cancer cell lines; this effect is thought to be mediated by the accumulation of malonyl-CoA in cells with upregulated FAS pathways. Toxicity Data
LD50: 547 mg/kg (oral, mouse) (A308)

[1]. Trans-chalcone and quercetin down-regulate fatty acid synthase gene expression and reduce ergosterol content in the human pathogenic dermatophyte Trichophyton rubrum. BMC Complement Altern Med. 2013 Sep 17;13:229.

[2]. Overexpression of steroidogenic acute regulatory protein in rat aortic endothelial cells attenuates palmitic acid-induced inflammation and reduction in nitric oxide bioavailability. Cardiovasc Diabetol. 2012 Nov 21;11:144.

[3]. Cerulenin blockade of fatty acid synthase reverses hepatic steatosis in ob/ob mice. PLoS One. 2013 Sep 27;8(9):e75980.

[4]. Fatty acid synthase inhibitor cerulenin inhibits topoisomerase I catalytic activity and augments SN-38-induced apoptosis. Apoptosis. 2013;18(2):226-237.

Cerulenin is an epoxydodecadecadiene amide isolated from various fungi, including Acremonium, Acrocylindrum, and Helicoceras. It inhibits the biosynthesis of various lipids by interfering with enzyme function. Cerulenin possesses a variety of activities, including antifungal, anti-infective, lipid-lowering, anti-metabolic, fatty acid synthesis inhibitory, and antibacterial activities. It is a monocarboxylic acid amide and epoxide. Cerulenin is an antifungal agent whose mechanism of action is through interfering with or preventing the formation of fatty acids and sterols. It has been reported that in fatty acid synthesis, Cerulenin binds to β-ketoacyl-ACP synthase in an equimolar ratio. In sterol synthesis, Cerulenin inhibits the activity of HMG-CoA synthase. Furthermore, Cerulenin has been shown to inhibit food intake in mice and lead to a significant decrease in their body weight. It is naturally found in Cephalosporium caerulens. Cerulenin has also been reported to be present in Cephalosporium caerulens and Euglena gracilis, with relevant data available.
Serunine is an antifungal antibiotic that inhibits the biosynthesis of sterols and fatty acids. Regarding fatty acid synthesis, it has been reported to bind to β-ketoacyl-ACP synthase in an equimolar ratio. Regarding sterol synthesis, it inhibits the activity of HMG-CoA synthase. It has also been shown to inhibit food intake in mice and cause significant weight loss. It is naturally found in Cephalosporium caerulens. [Wikipedia]
An epoxydodecadiene amide isolated from various fungi, including Acremonium, Acrocylindrum, and Helicoceras. It inhibits the biosynthesis of various lipids by interfering with enzyme function.

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Drug Indications
As a biochemical tool, serunine has been shown to cause significant weight loss in animals.

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Mechanism of Action
Serunine binds irreversibly to fatty acid synthases, particularly β-ketoacyl-acylcarrier protein synthases (FabH, FabB, and FabF condensates). Highly upregulated expression and activity of fatty acid synthase (FAS) have been observed in many tumor cells and cell lines. Cerulenin's inhibition of FAS leads to cytotoxicity and apoptosis in human cancer cell lines; this effect is thought to be mediated by the accumulation of malonyl-CoA in cells with upregulated FAS pathway.

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Pharmacodynamics
Cerulenin is an antifungal antibiotic isolated from Cyclocephalosporin. It blocks fungal growth by inhibiting the biosynthesis of sterols and fatty acids (inhibiting bacterial fatty acid synthesis). It also inhibits the activity of HMG-CoA synthase. Cerulenin produces metabolic effects similar to leptin, but its mechanism of action is independent of or downstream of leptin and melanocortin receptors.

C12H17NO3

223.27

223.12

17397-89-6

5282054

White to off-white solid powder

1.1±0.1 g/cm3

456.1±45.0 °C at 760 mmHg

93.5℃

241.1±25.0 °C

0.0±1.1 mmHg at 25°C

1.529

0.94

1

3

7

16

320

2

C/C=C/C/C=C/CCC(=O)[C@@H]1[C@@H](O1)C(=O)N

GVEZIHKRYBHEFX-NQQPLRFYSA-N

InChI=1S/C12H17NO3/c1-2-3-4-5-6-7-8-9(14)10-11(16-10)12(13)15/h2-3,5-6,10-11H,4,7-8H2,1H3,(H2,13,15)/b3-2+,6-5+/t10-,11-/m1/s1

(2R,3S)-3-[(4E,7E)-nona-4,7-dienoyl]oxirane-2-carboxamide

17397-89-6; Helicocerin; Cerulenin

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

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 (~447.89 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (11.20 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (11.20 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)