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
Irreversibly binds to fatty acid synthase, specifically b-ketoacyl-acyl carrier protein synthase (FabH, FabB and FabF condensation enzymes). A number of tumor cells and cell lines have been observed to have highly upregulated expression and activity of fatty acid synthase (FAS). Inhibition of FAS by cerulenin leads to cytotoxicity and apoptosis in human cancer cell lines, an effect believed to be mediated by the accumulation of malonyl-coenzyme A in cells with an upregulated FAS pathway.

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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 epoxydodecadienamide isolated from several species, including Acremonium, Acrocylindrum and Helicoceras. It inhibits the biosynthesis of several lipids by interfering with enzyme function. It has a role as an antifungal agent, an antiinfective agent, an antilipemic drug, an antimetabolite, a fatty acid synthesis inhibitor and an antimicrobial agent. It is a monocarboxylic acid amide and an epoxide.
Cerulenin is an antifungal agent whose activity interferes with or otherwise acts to prevent the formation of fatty acids and sterols. In fatty acid synthesis, reported to bind in equimolar ratio to b-keto-acyl-ACP synthase. In sterol synthesis, inhibits HMG-CoA synthetase activity. It is also shown to inhibit feeding and induce dramatic weight loss in mice. It is found naturally in the Cephalosporium caerulensfungus.
Cerulenin has been reported in Cephalosporium caerulens and Euglena gracilis with data available.
Cerulenin is an antifungal antibiotic that inhibits sterol and fatty acid biosynthesis. In fatty acid synthesis, reported to bind in equimolar ratio to b-keto-acyl-ACP synthase. In sterol synthesis, inhibits HMG-CoA synthetase activity. It is also shown to inhibit feeding and induce dramatic weight loss in mice. It is found naturally in the Cephalosporium caerulensfungus. [Wikipedia]
An epoxydodecadienamide isolated from several species, including ACREMONIUM, Acrocylindrum, and Helicoceras. It inhibits the biosynthesis of several lipids by interfering with enzyme function.

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Drug Indication
For use as a biochemical tool, Cerulenin is shown to cause dramatic weight loss in animals

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Mechanism of Action
Irreversibly binds to fatty acid synthase, specifically b-ketoacyl-acyl carrier protein synthase (FabH, FabB and FabF condensation enzymes). A number of tumor cells and cell lines have been observed to have highly upregulated expression and activity of fatty acid synthase (FAS). Inhibition of FAS by cerulenin leads to cytotoxicity and apoptosis in human cancer cell lines, an effect believed to be mediated by the accumulation of malonyl-coenzyme A in cells with an upregulated FAS pathway.

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Pharmacodynamics
Cerulenin is an antifungal antibiotic isolated from Cephalosporium caerulens. It interrupts fungal growth by inhibiting the biosynthesis of sterols and fatty acids (inhibits bacterial fatty acid synthesis). It also inhibits HMG-CoA synthetase activity. Cerulenin produces metabolic effects similar to effects of leptin, but through mechanisms that are independent of, or down-stream from, both 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.)