Novel Formulation of Undecylenic Acid induces Tumor Cell Apoptosis.

Undecylenic acid, a monounsaturated fatty acid, is currently in clinical use as a topical antifungal agent, however the potential for therapeutic application in other disease settings has not been investigated. In this study, we describe a novel platform for the solubilization of fatty acids using amino acids and utilize this approach to define a tumoricidal activity and underlying mechanism for undecylenic acid. We examined a novel formulation of undecylenic acid compounded with L-Arginine, called GS-1, that induced concentration-dependent tumor cell death, with undecylenic acid being the cytotoxic component. Further investigation revealed that GS-1-mediated cell death was caspase-dependent with a reduction in mitochondrial membrane potential, suggesting a pro-apoptotic mechanism of action. Additionally, GS-1 was found to localize intracellularly to lipid droplets. In contrast to previous studies where lipid droplets have been shown to be protective against fatty acid-induced cell death, we showed that lipid droplets could not protect against GS-1-induced cytotoxicity. We also found a role for Fatty Acid Transport Protein 2 (FATP2) in the uptake of this compound. Collectively, this study demonstrates that GS-1 has effective pro-apoptotic antitumor activity in vitro and, together with the novel platform of fatty acid solubilization, contributes to the re-emerging field of fatty acids as potential anti-cancer therapeutics.

Highly Active, Entirely Biobased Antimicrobial Pickering Emulsions.

We present the development of surfactant-free, silica-free and fully biobased oil-in-water antimicrobial Pickering emulsions, based on the self-assembly of ß-cyclodextrin and phytoantimicrobial oils (terpinen-4-ol or carvacrol). Undecylenic acid (UA), derived from castor oil, can be used as bio-based drug to treat fungal infection, but is less effective than petroleum-based drugs as azole derivatives. To maximize its antifungal potential, we have incorporated UA in fully biobased Pickering emulsions. These emulsions are effective against fungi, Gram-positive and Gram-negative bacteria. The carvacrol emulsion charged with UA is +390 % and +165 % more potent against methicillin-resistant S. aureus (MRSA), compared to UA and azole-based commercial formulations. Moreover, this emulsion is up to +480 % more efficient that UA ointment against C. albicans. Finally, remarkable eradication of E. coli and MRSA biofilms was obtained with this environmental-friendly emulsion.

Molecular modeling and phenoloxidase inhibitory activity of arbutin and arbutin undecylenic acid ester.

Excessive melanin formation has been linked to various skin disorders such as hyperpigmentation and skin cancer. Tyrosinase is the most prominent target for inhibitors of melanin production. In this study, we investigated whether arbutin and its prodrug, arbutin undecylenic acid ester, might inhibit phenoloxidase (PO), a tyrosinase-like enzyme. Molecular docking simulation results suggested that arbutin and arbutin undecylenic acid ester can bind to the substrate-binding pocket of PO. Arbutin undecylenic acid ester with an IC50 6.34 mM was effective to inhibit PO compared to arbutin (IC50 29.42 mM). In addition, arbutin undecylenic acid ester showed low cytotoxicity in Drosophila S2 cells and the compound inhibited the melanization reaction. Therefore, the results of this study have demonstrated that arbutin undecylenic acid ester as a potential inhibitor of PO. We successfully designed a new platform utilizing Drosophila melanogaster and Bombyx mori as animal models propounding fast, cheap, and high effectiveness in method to screen tyrosinase inhibitors.

Effect of Polyhexamethylene Biguanide in Combination with Undecylenamidopropyl Betaine or PslG on Biofilm Clearance.

Hospital-acquired infection is a great challenge for clinical treatment due to pathogens' biofilm formation and their antibiotic resistance. Here, we investigate the effect of antiseptic agent polyhexamethylene biguanide (PHMB) and undecylenamidopropyl betaine (UB) against biofilms of four pathogens that are often found in hospitals, including Gram-negative bacteria Pseudomonas aeruginosa and Escherichia coli, Gram-positive bacteria Staphylococcus aureus, and pathogenic fungus, Candida albicans. We show that 0.02% PHMB, which is 10-fold lower than the concentration of commercial products, has a strong inhibitory effect on the growth, initial attachment, and biofilm formation of all tested pathogens. PHMB can also disrupt the preformed biofilms of these pathogens. In contrast, 0.1% UB exhibits a mild inhibitory effect on biofilm formation of the four pathogens. This concentration inhibits the growth of S. aureus and C. albicans yet has no growth effect on P. aeruginosa or E. coli. UB only slightly enhances the anti-biofilm efficacy of PHMB on P. aeruginosa biofilms. However, pretreatment with PslG, a glycosyl hydrolase that can efficiently inhibit and disrupt P. aeruginosa biofilm, highly enhances the clearance effect of PHMB on P. aeruginosa biofilms. Meanwhile, PslG can also disassemble the preformed biofilms of the other three pathogens within 30 min to a similar extent as UB treatment for 24 h.

ω-hydroxyundec-9-enoic acid induction of breast cancer cells apoptosis through generation of mitochondrial ROS and phosphorylation of AMPK.

This study was performed to evaluate the anticancer effect of ω-hydroxyundec-9-enoic acid (ω-HUA), a microbial bio-catalyst product in breast cancer cells, through AMP-activated protein kinase (AMPK) regulation. ω-HUA mediated apoptosis was induced in breast cancer cells by AMPK activation, loss of mitochondrial membrane potential, and reactive oxygen species (ROS) generation. ω-HUA treatment of breast cancer cells increased the AMPK phosphorylation levels, cleaved caspase-3, and poly (ADP-ribose) polymerase (PARP) proteins. In addition, anti-apoptotic members, such as Bcl-2, were downregulated, while Bax, a pro-apoptotic member, was upregulated. ω-HUA decreased the mitochondrial membrane potential while increasing the expression of cytochrome c (cyt c). Treating the cells with compound C, an AMPK inhibitor, reversed the phenomena, leading to an increase in cell viability and a decrease in apoptosis induction. Treating the cells with an ROS scavenger, N-acetyl cysteine (NAC), led to AMPK inactivation and apoptosis inhibition, allowing the recovery of cell health. In conclusion, ω-HUA sequentially caused the production of mitochondrial ROS and the consequent AMPK activation, thereby inducing apoptosis in breast cancer cells. Thus, ω-HUA may prove useful as an anticancer agent that targets AMPK in breast cancer cells.

Identification and characterization of Zika virus NS5 RNA-dependent RNA polymerase inhibitors.

The current outbreak of Zika virus (ZIKV) is the impetus for novel, safe and efficacious anti-ZIKV agents. ZIKV non-structural protein 5 RNA-dependent RNA polymerase (RdRp) is essential for viral replication and is logically regarded as an attractive drug target. This study used a fluorescence-based polymerase assay to find an anti-infective drug 10-undecenoic acid zinc salt (UA) which could inhibit RdRp activity with a half maximal inhibitory concentration (IC50) of 1.13-1.25 µM. Molecular docking and site-directed mutagenesis analyses identified D535 as the key amino acid in the interaction between RdRp and UA. Importantly, the surface plasmon resonance assay showed that UA had strong direct binding with ZIKV wild-type RdRp and a relatively weak interaction with D535A-RdRp. As a control, the nucleoside inhibitor sofosbuvir triphosphate (PSI-7409) conferred insensitivity to the fluorescence-based RdRp assay and cannot bind directly with RdRp. Moreover, UA showed anti-ZIKV activity comparable to sofosbuvir. All these results indicate that UA is likely to be a promising lead compound against ZIKV, exhibiting a different mechanism than sofosbuvir.

Identification of undecylenic acid as EAG channel inhibitor using surface plasmon resonance-based screen of KCNH channels.

BACKGROUND: KCNH family of potassium channels is responsible for diverse physiological functions ranging from the regulation of neuronal excitability and cardiac contraction to the regulation of cancer progression. KCNH channels contain a Per-Arn-Sim (PAS) domain in their N-terminal and cyclic nucleotide-binding homology (CNBH) domain in their C-terminal regions. These intracellular domains shape the function of KCNH channels and are important targets for drug development. METHODS: Here we describe a surface plasmon resonance (SPR)-based screening method aimed in identifying small molecule binders of PAS and CNBH domains for three KCNH channel subfamilies: ether-à-go-go (EAG), EAG-related gene (ERG), and EAG-like K+ (ELK). The method involves purification of the PAS and CNBH domains, immobilization of the purified domains on the SPR senor chip and screening small molecules in a chemical library for binding to the immobilized domains using changes in the SPR response as a reporter of the binding. The advantages of this method include low quantity of purified PAS and CNBH domains necessary for the implementation of the screen, direct assessment of the small molecule binding to the PAS and CNBH domains and easiness of assessing KCNH subfamily specificity of the small molecule binders. RESULTS: Using the SPR-based method we screened the Spectrum Collection Library of 2560 compounds against the PAS and CNBH domains of the three KCNH channel subfamilies and identified a pool of small molecules that bind to the PAS or CNBH domains. To further evaluate the effectiveness of the screen we tested the functional effect of one of the identified mEAG PAS domain specific small molecule binders on currents recorded from EAG channels. Undecylenic acid inhibited currents recorded from EAG channels in a concentration-dependent manner with IC50 of ~ 1 µM. CONCLUSION: Our results show that the SPR-based method is well suited for identifying small molecule binders of KCNH channels and can facilitate drug discovery for other ion channels as well.

Evaluating the Effects of a Topical Preparation with Dexpanthenol, Silbiol, Undecylenic Acid, and Lidocaine on Palatal Mucosa Wound Healing in a Rat Model

Background: Postoperative complications occur after periodontal plastic surgeries, but an ideal treatment to overcome them has not been found yet. Aims: To evaluate the effects of topically applied Oral-norm gel on the healing of excisional wounds. Study Design: Animal experiment. Methods: Excisional wounds with a diameter of 3 mm were made in the center of the palatal mucosa of 63 Sprague Dawley rats. Seven animals were sacrificed at time 0. The remaining rats were divided into two groups: a test group in which the topical Oral-norm gel was applied three times a day and a control group in which nothing was applied. Seven animals in each group were sacrificed at 3, 7, 14, and 21 days. Mean wound surface area was measured photographically, while wound healing and width were evaluated microscopically. Results: The mean wound surface area decreased significantly after 3 days in both groups (p<0.001). Between days 3 and 7, the mean wound surface area decreased from 6.62 (2.85) to 0.83 (1.62) mm2 in the control group and 5.07 (0.88) to 1.42 (1.67) mm2 in the test group. The wound width decreased significantly on day 7 in both groups (p<0.001), with no further changes by day 14. Both groups had a significant increase in inflammation and vascularization on day 3 (p<0.001), with a reduction thereafter. No significant differences in macroscopic and microscopic measurements were observed between the groups at any time point (p>0.05). Conclusion: The Oral-norm gel has no positive healing effects in the palatal mucosa of rats.

ω-hydroxyundec-9-enoic acid induces apoptosis by ROS mediated JNK and p38 phosphorylation in breast cancer cell lines.

ω-Hydroxyundec-9-enoic acid (ω-HUA), a plant secondary metabolite, exhibits anti-fungal activity. However, its effect on breast cancer cells is unknown. Here, we investigated the anti- breast cancer activity of ω-HUA and its underlying mechanism. Treatment of human breast cancer cell lines, MDA-MB-231 and MDA-MB-435, with ω-HUA induced apoptotic cell death with increased cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP) levels, and p38 and JNK phosphorylation. Inhibition of these mitogen-activated protein kinase (MAPK) pathways using specific inhibitors or siRNA, for p38 and JNK, respectively, blocked the ω-HUA-induced apoptosis in a dose-dependent manner. Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited ω-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability. MDA-MB-231 xenograft model showed that the ω-HUA-treated group exhibited greater tumor regression and significantly reduced tumor weight compared to that exhibited by the vehicle-administered group. Collectively, ω-HUA-induced intracellular ROS generation induced breast cancer cell apoptosis through JNK and p38 signaling pathway activation, resulting in tumor regression. The results suggested that ω-HUA is an effective supplement for inhibiting human breast cancer growth.

Preparation and biocompatibility of crosslinked poly(3-hydroxyundecenoate).

A sticky polymer, poly(3-hydroxyundecenoate) (PHU), was produced by Pseudomonas oleovorans when nonanoate and undecenoate were used as carbon sources. Crosslinked PHU (CL-PHU) was prepared by heating using benzoyl peroxide as a crosslinker. According to the degree of crosslinking in the polymer, three types of CL-PHU were prepared: CL-PHU50, CL-PHU60 and CL-PHU70. Fourier transform-infrared spectroscopy, thermogravimetric analysis, and differential scanning calorimetry results suggested that crosslinking of PHU was successfully achieved by heat, which increased the crosslinking density and decreased stiffness and flexibility of the polymer. Water contact angle measurements revealed no differences of hydrophilicity as the crosslinking density. Slight morphological changes of CL-PHU film surfaces were observed by atomic force microscopy. Chinese hamster ovary cells were used to investigate the biocompatibility of CL-PHU films using poly(l-lactide) surfaces as control. Surface properties of the film, such as roughness and adhesive force, enhanced the adhesion and proliferation of cells on the films. CL-PHU might be useful for cell compatible biomedical applications.

Antifungal effects of undecylenic acid on the biofilm formation of Candida albicans.

Undecylenic acid can effectively control skin fungal infection, but the mechanism of its fungal inhibition is unclear. Hyphal growth of Candida albicans (C. albicans) and biofilm formation have been well recognized as important virulence factors for the initiation of skin infection and late development of disseminated infection. In this study, we seek to investigate antifungal mechanisms of undecylenic acid by evaluating the virulence factors of C. albicans during biofilm formation. We found that undecylenic acid inhibits biofilm formation of C. albicans effectively with optimal concentration above 3 mM. In the presence of this compound, the morphological transition from yeast to filamentous phase is abolished ultimately when the concentration of undecylenic acid is above 4 mM. Meanwhile, the cell surface is crumpled, and cells display an atrophic appearance under scanning electron microscopy even with low concentration of drug treatment. On the other hand, the drug treatment decreases the transcriptions of hydrolytic enzymes such as secreted aspartic protease, lipase, and phospholipase. Hyphal formation related genes, like HWP1, are significantly reduced in transcriptional level in drug-treated biofilm condition as well. The down-regulated profile of these genes leads to a poorly organized biofilm in undecylenic acid treated environment.

Polyelectrolyte-coated nanocapsules containing undecylenic acid: Synthesis, biocompatibility and neuroprotective properties.

The main objectives of the present study were to investigate the biocompatibility of polyelectrolyte-coated nanocapsules and to evaluate the neuroprotective action of the nanoencapsulated water-insoluble neuroprotective drug-undecylenic acid (UDA), in vitro. Core-shell nanocapsules were synthesized using nanoemulsification and the layer-by-layer (LbL) technique (by saturation method). The average size of synthesized nanocapsules was around 80 nm and the concentration was 2.5 × 10(10) particles/ml. Their zeta potential values ranged from less than -30 mV for the ones with external polyanion layers through -4 mV for the PEG-ylated layers to more than 30 mV for the polycation layers. Biocompatibility of synthesized nanocarriers was evaluated in the SH-SY5Y human neuroblastoma cell line using cell viability/toxicity assays (MTT reduction, LDH release). The results obtained showed that synthesized nanocapsules coated with PLL and PGA (also PEG-ylated) were non-toxic to SH-SY5Y cells, therefore, they were used as nanocarriers for UDA. Moreover, studies with ROD/FITC-labeled polyelectrolytes demonstrated approximately 20% cellular uptake of synthetized nanocapsules. Further studies showed that nanoencapsulated form of UDA was biocompatible and protected SH-SY5Y cells against the staurosporine-induced damage in lower concentrations than those of the same drug added directly to the culture medium. These data suggest that designed nanocapsules might serve as novel, promising delivery systems for neuroprotective agents.

Efficacious intestinal permeation enhancement induced by the sodium salt of 10-undecylenic acid, a medium chain fatty acid derivative.

10-undecylenic acid (UA) is an OTC antifungal therapy and a nutritional supplement. It is an unsaturated medium chain fatty acid (MCFA) derivative, so our hypothesis was that its 11-mer sodium salt, uC11, would improve intestinal permeation similar to the established enhancer, sodium caprate (C10), but without the toxicity of the parent saturated MCFA, decylenic acid (C11). MTT assay and high-content screening (HCS) confirmed a cytotoxicity ranking in Caco-2 cells: C11 > C10 = uC11. Five to ten millimolars of the three agents reduced TEER and increased the Papp of [(14)C]-mannitol across Caco-2 monolayers and rat intestinal mucosae, a concentration that matched increases in plasma membrane permeability seen in HCS. Although C11 was the most efficacious enhancer in vitro, it damaged monolayers and tissue mucosae more than the other two agents at similar concentrations and exposure times and was therefore not pursued further. Rat jejunal and colonic in situ intestinal instillations of 100 mM C10 or uC11 with FITC-dextran 4000 (FD4) solutions yielded comparable regional enhancement ratios of ~10 and 30%, respectively, for each agent with acceptable tissue histology. Mini-tablets of uC11 and FD4 however delivered more FD4 compared to C10-FD-4 mini-tablets in both regions, as reflected by a statistically higher AUC, and with no evidence of membrane perturbation. The unsaturated bond in uC11 therefore confers a reduction in lipophilicity and cytotoxicity compared to C11, and the resulting permeation enhancement is on a par with or superior to that of C10, a key component of formulations in current phase II oral peptide clinical trials.

ω-Hydroxyundec-9-enoic acid induces apoptosis through ROS-mediated endoplasmic reticulum stress in non-small cell lung cancer cells.

ω-Hydroxyundec-9-enoic acid (ω-HUA), a hydroxyl unsaturated fatty acid derivative, is involved in the antifungal activity of wild rice (Oryza officinalis). Here, we investigated the anti-cancer activity of ω-HUA on a non-small cell lung cancer (NSCLC) cell line. ω-HUA increased apoptosis and induced cleavages of caspase-6, caspase-9, and poly (ADP-ribose) polymerase (PARP). ω-HUA treatment significantly induced endoplasmic reticulum (ER) stress response. Suppression of CHOP expression and inhibiting ER stress by 4-phenylbutyrate (4-PBA) significantly attenuated the ω-HUA treatment-induced activation of caspase-6, caspase-9, and PARP, and subsequent apoptotic cell death, indicating a role for ER stress in ω-HUA-induced apoptosis. In addition, cells subjected to ω-HUA exhibited significantly increased quantity of reactive oxygen species (ROS), and the ROS scavenger N-acetyl-L-cysteine (NAC) inhibited ω-HUA-induced apoptotic cell death and ER stress signals, indicating a role for ROS in ER stress-mediated apoptosis in ω-HUA-treated cells. Taken together, these results suggest that sequential ROS generation and ER stress activation are critical in ω-HUA treatment-induced apoptosis and that ω-HUA represents a promising candidate for NSCLC treatment.

Thermoplastic polyurethanes from undecylenic acid-based soft segments: structural features and release properties.

A set of thermoplastic polyurethanes is synthesized, combining undecylenic acid-derived telechelic diols as soft segments and 1,4-butanediol/4,4'-methylenebis(phenylisocyanate) as a hard segment (HS). These polymers are fully chemically and physically characterized by means of NMR and Fourier transform IR (FTIR) spectroscopy, size-exclusion chromatography (SEC), DSC, thermogravimetric analysis (TGA), tensile testing, and contact angle measurements. The obtained results reveal that both the molecular weight of the diol and the HS content greatly influence the physical and mechanical properties of these polymers. In addition, given the potential use of these materials for biomedical applications, hydrolytic degradation, their biocompatibility using a human fibroblast cell line, and performance as drug delivery carriers are evaluated.

Effects of undecylenic acid released from denture liner on Candida biofilms.

Denture liners (DL) are easily colonized by Candida spp. In an attempt to prevent biofilm colonization, manufacturers have incorporated undecylenic acid (UDA) into DL. In this in vitro study, the effects of UDA released from DL on Candida biofilms were investigated. The concentrations of UDA released from commercial DL were determined by gas chromatography-mass spectrometry (GC-MS). Minimum inhibitory concentration (MIC) and minimum fungistatic concentration (MFC) tests were performed for C. albicans or C. glabrata, with UDA for comparison with the concentrations released from DL. Specimens of DL with (experimental group) and without UDA (control group) were fabricated, and Candida biofilms were developed on DL surfaces. Biofilms were evaluated by cell counts, metabolic activity, structure, and secretion of proteinase or phospholipase. The concentrations of UDA released were within the MIC and MFC ranges. In the presence of UDA, C. albicans biofilms were thinner and had lower numbers of viable and active cells, although no significant enzymatic changes were observed relative to the control group (p > 0.05). In contrast, C. glabrata biofilms exhibited higher cell counts and greater metabolic activity and also increased proteinase activity in the presence of UDA relative to the control group (p < 0.05). Overall, UDA did not prevent Candida biofilm formation.

Neuroprotective effect of undecylenic acid extracted from Ricinus communis L. through inhibition of µ-calpain.

The key neuropathological features of Alzheimer's disease are abnormal deposition of Aß plaques and insoluble Aß peptides in extracellular brain and intracellular neurofibril tangles induced by abnormal tau hyperphosphorylation. µ-Calpain is one of the factors that bridge these Aß- and hyperphosphorylated tau-mediated pathological pathways. Undecylenic acid (UDA), a naturally occurring unsaturated fatty acid, was discovered as a µ-calpain inhibitor by screening a chemical library using a substrate specific µ-calpain assay method. UDA inhibited Aß oligomerization and Aß fibrillation and reversed Aß-induced neuronal cell death. In addition, UDA scavenged ROS and reversed the levels of proapoptotic proteins induced by ROS in SH-SY5Y cells. UDA inhibited µ-calpain activity with better potency than the known peptide-like µ-calpain inhibitor, MDL28170, in SH-SY5Y and HEK293T cells transfected with the catalytic subunit of µ-calpain. These results suggest that UDA is a novel non-peptide-like µ-calpain inhibitor with good cell permeability and potent neuroprotective effect.

Anti-inflammatory properties of a new undecyl-rhamnoside (APRC11) against P. acnes.

Acne vulgaris is a skin disease affecting pilosebaceous glands in which Propionibacterium acnes (P. acnes) induced inflammation plays a central role. In order to develop new therapies against the inflammatory events, we evaluated the modulating effect of a new undecyl-rhamnoside, APRC11, on different markers of the inflammation. For this purpose, normal human keratinocytes taken from five healthy donors were pre-incubated for 24 h with APRC11 or Zinc Gluconate (Zn) which was used as reference molecule for its anti-inflammatory properties. Then, keratinocytes were stimulated with P. acnes Membrane Fraction for 6 h, in the presence of either APRC11 or Zn. Different markers were evaluated at mRNA level using a Luminex-based Quantigene array system and at protein level using an ELISA test and a Luminex array system. Results showed that P. acnes significantly increased the expression of IL-1α, IL-1RA, IL-8 and MMP-9. A 24-h treatment with APRC11 prior to the P. acnes stimulation down-regulated the P. acnes-induced cytokines over expression (IL-1α, IL-8 and MMP-9) and up-regulated IL-1RA level in a similar manner than Zn. These regulations were noted at both protein and mRNA levels. In conclusion, the new undecyl-rhamnoside APRC11 is able to down-regulate the expression of molecules implicated in cutaneous inflammation and whose expression is induced by P. acnes, confirming its potential interest in inflammatory acne.

Stimulatory effect of undecylenic acid on mouse osteoblast differentiation.

Natural compounds with bone-forming (or anabolic) activity have been recently focused on in bone research. The present study investigated the effect of undecylenic acid (UA) on osteoblast differentiation in mouse osteoblastic MC3T3-E1 subclone 4 cells and primary mouse calvarial cells. Low concentrations of UA (up to 5 microM) exhibited no cytotoxicity and significantly increased the expression and activity of alkaline phosphatase (early differentiation marker of osteoblast) and calcium deposition with the induction of expression of the osteocalcin gene in both cells. Interestingly, at low concentration of UA, the induction of NF-kappaB p65 translocation into nucleus and the up-regulation of AP-1 and NFATc1 transcript levels were also observed, suggesting that the stimulatory effect of UA on osteoblast differentiation could be mediated through the activation of transcription factors. Additionally, although the patterns of UA-induced activation of MAP kinases (JNK and p38) were not completely consistent with the increase of both ALP activity and calcium deposition by UA, MAP kinases might be partially involved in the biological function of UA during the early and late stages of osteoblast differentiation.

Undecylenic acid: a valuable and physiologically active renewable building block from castor oil.

A lot of attention is currently being paid to the transition to a biobased economy. In this movement, most efforts concentrate on the development of bioenergy applications including bioethanol, biodiesel, thermochemical conversion of biomass, and others. However, in the energy sector other nonbiomass alternatives are known, whereas no valuable alternatives are available when thinking about chemical building blocks. Therefore, it is also essential to develop new routes for the synthesis of bio-based chemicals and materials derived thereof. Such intermediates can originate either from plants or from animals. Castor oil is a non-edible oil extracted from the seeds of the castor bean plant Ricinus communis (Euphorbiaceae), which grows in tropical and subtropical areas. Globally, around one million tons of castor seeds are produced every year, the leading producing areas being India, PR China, and Brazil.2 10-Undecenoic acid or undecylenic acid is a fatty acid derived from castor oil that, owing to its bifunctional nature, has many possibilities to develop sustainable applications.