Background Scarring typically occurs after trauma, burn injury or surgery. Hypertrophic scarring presents as raised, red and itchy lesions which variably respond to various treatment modalities, such as corticosteroids, pressure garments, laser therapy, the use of silicone sheets and radiotherapy.
Kynurenine, or "Fibrostop 1" (FS1), and its further breakdown products, such as kynurenic acid, or "Fibrostop 2" (FS2), are endogenous products found in many systems and have shown potential in reducing scar formation in animal studies.
The aim of study is to evaluate the safety and tolerability of FS2 cream applied to the skin of healthy human subjects.

Start Date01 May 2015

Sponsor / Collaborator-

100 Clinical Results associated with Kynurenic acid

100 Translational Medicine associated with Kynurenic acid

100 Patents (Medical) associated with Kynurenic acid

1,906

Literatures (Medical) associated with Kynurenic acid

01 Mar 2025·Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy

Prediction of total lipids and fatty acids in black soldier fly (Hermetia illucens L.) dried larvae by NIR-hyperspectral imaging and chemometrics

Article

Author: Barbin, Douglas Fernandes ; Cruz-Tirado, J P ; Dos Santos Vieira, Matheus Silva ; Batista, Eduardo Augusto Caldas ; Ferreira, Ramon Sousa Barros ; Amigo, José Manuel

The unique fatty acid composition of BSF larvae oil makes it suitable for various applications, including use in animal feed, aquaculture, biodiesel production, biomaterials, and the food industry. Determination of BSF larvae composition usually requires analytical methods with chemicals, thus needing emerging techniques for fast characterization of its composition. In this study, Near Infrared Hyperspectral Imaging (NIR-HSI) (928 - 2524 nm) coupled with chemometrics was applied to predict the lipid content and fatty acid composition in intact black soldier fly (BSF) larvae. Partial Least Squares Regression (PLSR) and Support Vectors Machine Regression (SVMR) models, combined with two variable selection methods, Interval Partial Least Squares (iPLS) and Bootstrapping Soft Shrinkage (BOSS), were compared. PLSR reached a good performance to predict myristic acid with Root Mean Square Error in prediction (RMSEP) = 0.45 %, while SVMR reached values of Ratio to Prediction Deviation (RPD) > 3 to predict total lipid content, lauric acid, myristic acid, palmitic acid and oleic acid. In addition, selecting wavelength by BOSS improved PLSR models (6 - 15 % increases in RPD), while iPLS improved SVMR model to predict palmitic acid (16 % increases in RPD). The study emphasizes the advantages of NIR-HSI as a non-invasive, rapid method for lipid and fatty acid quantification, which can be highly valuable for industrial applications such as monitoring BSF larvae feeding systems to ensure high-quality oil production.

01 Mar 2025·Physiology & Behavior

Role of glutamatergic signaling in the acquisition and expression of learned sugar preferences in C57BL/6 mice

Article

Author: Rayman, Nareesa ; Bodnar, Richard J ; Sarker, Joymin ; Carata, Ion ; Pines, Rachel ; Narine, Shania ; Castillo, Alexander ; Limbu, Brian ; Sclafani, Anthony ; Bochner, Yerachmiel

C57BL/6 (B6) mice learn to prefer glucose or sucrose to initially isopreferred or even more preferred nonnutritive sweeteners due to the postoral appetite stimulating (appetition) actions of glucose. Recent evidence indicates that specific duodenal neuropod cells transmit the glucose appetition signal to the brain via glutamatergic synaptic connections with vagal afferents. The present study found that intraperitoneal pretreatment with a glutamatergic receptor antagonist cocktail (kynurenic acid (KA)/D-2-amino-3-phosphonopentanoic acid (AP3)) in B6 mice did not block the expression of their learned preference for 8% glucose solution over an initially-preferred 0.1% sucralose + 0.1% saccharin solution. However, acquisition of the glucose preference was blocked by drug treatment during 1-h training sessions with the two sweeteners. Systemic KA/AP3 injections also did not block the expression of the learned preference for a 10.6% sucrose solution over a 0.6% sucralose solution. Drug effects on the acquisition of the sucrose preference were not determined because sucrose, unlike glucose conditioning, required 24-h training trials. The findings that the 1-h training regimen conditioned 8% glucose, but not 10.6% sucrose, preferences suggest that glucose has more potent appetition actions. This was confirmed by the finding that B6 mice learned to prefer 10.6% glucose to 10.6% sucrose after 1-h or 24-h training despite an initial strong sucrose preference. This action can be explained by 10.6% sucrose's digestion in the gut to glucose and fructose with only glucose activating the gut-brain appetition pathway.

01 Mar 2025·Journal of Hazardous Materials

Prenatal amoxicillin exposure induces depressive-like behavior in offspring via gut microbiota and myristic acid-mediated modulation of the STING pathway

Article

Author: Xu, Dan ; Luo, Mingcui ; Wang, Hui ; Wang, Tingting ; Lu, Mengxi ; Jin, Xiuping ; Guo, Juanjuan ; Zhou, Xinli ; Qi, Cuiping ; Chen, Huijun ; Wei, Liyi

Amoxicillin is a widely used antibiotic globally, and its pervasive environmental presence poses significant risks to human health and ecosystems. Notably, prenatal amoxicillin exposure (PAmE) may have long-term neurodevelopmental toxicity for offspring. In this study, we investigated the lasting effects of PAmE on depressive-like behaviors in offspring rats, emphasizing the biological mechanisms mediated by changes in gut microbiota and its metabolite, myristic acid. Our results showed that PAmE significantly disrupted the gut microbiota composition in offspring, particularly through the reduction of Lachnospiraceae, leading to decreased levels of myristic acid. This disruption hindered the N-myristoylation of ADP-ribosylation factor 1 (ARF1), impaired the normal degradation of the stimulator of interferon genes protein, inhibited autophagic processes, and promoted M1 polarization of microglia, ultimately leading to depressive-like behaviors in the offspring. Remarkably, supplementation with Lachnospira or myristic acid effectively reversed the PAmE-induced neurodevelopmental and behavioral abnormalities, alleviating depressive-like symptoms. This study reveals how PAmE affects offspring neurodevelopment and behavior through gut microbiota and myristic acid, highlighting the crucial role of the gut-brain axis in the modulation of depressive symptoms. Supplementing Lachnospira or myristic acid could represent a novel strategy to mitigate PAmE-induced fetal-originated depression, providing new biological evidence and potential therapeutic avenues.

News (Medical) associated with Kynurenic acid

20 Dec 2024

·www.globenewswire.com

Kynexis Announces Positive Topline Results from Phase 1 Study of KYN-5356, a Potential Treatment for Cognitive Impairment Associated with Schizophrenia

KYN-5356, an innovative, first-in-class small molecule inhibitor of KAT-II, a key enzyme in the kynurenine pathway implicated in schizophrenia, was shown to be safe and well-tolerated in the phase 1 study in healthy volunteers Initial data show clear evidence of target engagement and suggestive evidence of cognitive improvement, adding to body of evidence that supports further study of KYN-5356 in patients with cognitive impairment associated with schizophrenia (CIAS), which is among the most debilitating symptoms of the disease Clinical trial in patients anticipated to begin in 2025 Dec. 17, 2024 -- Kynexis, a biotechnology company focused on precision therapeutics for brain diseases, today announced positive topline results from its first-in-human phase 1 clinical trial. The phase 1 study in healthy volunteers evaluated the safety, tolerability, and pharmacokinetics of single and multiple ascending oral doses of KYN-5356, a first-in-class small molecule inhibitor of KAT-II, being developed for the treatment of cognitive impairment associated with schizophrenia (CIAS). The study also evaluated central pharmacodynamic biomarkers and cognitive performance to determine target engagement in the multiple ascending part. Results show that KYN-5356 was safe and well-tolerated and exhibited excellent pharmacokinetic (PK) properties in both plasma and cerebrospinal fluid (CSF), suggesting appropriate penetration and exposure of KYN-5356 in the central nervous system (CNS). The study also tested exploratory pharmacodynamic (PD) endpoints, where KYN-5356 demonstrated statistically significant improvements in electroencephalography (EEG) activity relevant to cognitive pathways, as well as early, suggestive evidence of cognitive improvement. Findings further showed a dose-dependent reduction of kynurenic acid levels in the CSF, which have been shown to be elevated in people with schizophrenia and are believed to be a key driver of CIAS. “Cognitive impairment is a primary driver of disability for people with schizophrenia and affects most people with the disease. While still early, these data represent a milestone for Kynexis as we advance this potentially first-in-class treatment for cognitive impairment associated with schizophrenia, or CIAS,” said Kees Been, Chief Executive Officer of Kynexis. “As the first KAT-II inhibitor studied in humans, KYN-5356 has demonstrated an excellent safety profile and promising pharmacokinetic data, including evidence of significant brain penetration. The observed dose-dependent reductions in CSF kynurenic acid levels, the effects on EEG activity, and the early evidence of cognitive benefit further validate our precision-medicine approach to targeting the kynurenine pathway for CIAS.” Dr. Jens Wendland, Chief Medical Officer at Kynexis, continued, “All subjects successfully completed the study, and the data provide critical insights into the brain effects of KYN-5356. These findings, including data showing clear target engagement across several biomarker modalities, build on the body of evidence supporting its potential to treat cognitive impairment associated with schizophrenia. We look forward to sharing the full phase 1 results at a scientific conference next year and are now moving swiftly toward initiating our first-in-patient clinical study in 2025.” Kynexis is advancing precision therapeutics for brain diseases by taking a biomarker-based approach to advance a potential treatment for cognitive impairment associated with schizophrenia (CIAS). By harnessing large data to identify and stratify patients based on the underlying causal human biology of the disease, Kynexis is targeting KAT-II, a key enzyme in the kynurenine pathway. The company’s lead candidate, KYN-5356, is a first-in-class small molecule that is potent and highly selective for KAT-II. The Company has a subsidiary in the United States, which is based in Cambridge, Mass. (Kynexis Therapeutics Inc.). Learn more at kynexistx.com and follow us on LinkedIn and X.: The content above comes from the network. if any infringement, please contact us to modify.

Clinical Result

15 Dec 2023

·www.prnewswire.com

Three Articles in the Journal of Pharmaceutical Analysis Uncover Previously Unknown Drug and Disease Mechanisms

Researchers identify promising treatment candidates for morphine tolerance and cancer, as well as a biomarker for kidney injury. XI'AN, China, Dec. 15, 2023 /PRNewswire/ -- Long-term use of analgesics such as morphine leads to "tolerance" that reduces drug efficacy. In such cases, dose escalation may be required to achieve the same analgesic effects. The key molecular mechanism of morphine tolerance is its inefficiency in inducing mu-opioid receptor (MOR) endocytosis. None of the currently available strategies to counter morphine tolerance address this underlying molecular mechanism. Moreover, understanding how drugs work is crucial to determine their efficacy. There is also an unmet need for new diagnostic biomarkers that can help identify diseases at an early stage. The October issue of JPA features three articles that address these issues and systematically lay a foundation for future studies and treatment strategies. Continue Reading Opioids, including morphine, are frequently used for managing chronic pain. However, long-term use of morphine leads to tolerance, resulting in reduced analgesic efficacy. The first study aimed to address the issue of morphine tolerance by developing a monoclonal antibody (mAb) named 3A5C7 that precisely targets MOR. The therapeutic efficacy of 3A5C7 and its underlying molecular mechanisms were also evaluated as part of the study. The article was available online in June 2023 and published in Volume 13, Issue 10 in October 2023. The results showed that cell lines HEK293T and SH-SY5Y treated with 3A5C7 exhibited enhanced morphine-induced MOR endocytosis and recycling from cytoplasm to plasma membrane. Further, 3A5C7 diminished hyperactivation of adenylate cyclase, an in vitro biomarker of morphine tolerance. Finally, chronic intrathecal 3A5C7 administration significantly alleviated morphine tolerance in mice, while both chronic and acute 3A5C7 intrathecal administration attenuated morphine dependence. Corresponding author Prof. Zhi-Nan Chen states, "Our newly developed mAb targets MOR with high affinity and specificity, and alleviates morphine tolerance and physical dependence, offering a new therapeutic strategy in the management of chronic pain." In the second study, researchers dug deeper into the anticancer mechanisms of the drug 'pracinostat,' which is a histone deacetylase inhibitor (HDACi). Findings revealed that pracinostat exerts its antitumor effects by inducing excessive asymmetric mitochondrial fission in tumor cells. It switches the scission position from the mitochondrial midzone to the periphery and leads to the selective cell death of tumor cells with high cyclin-dependent kinase 5 (CDK5) levels, representing a promising strategy for anticancer therapy. "Our results revealed the anticancer mechanism of the HDACi pracinostat in colorectal cancer (CRC) via the activation of CDK5-Drp1 signaling to cause selective mitofission-associated cell death (MFAD) of CDK5-high tumor cells, which implicates a new paradigm to develop potential therapeutic strategies for CRC treatment," explains the corresponding author Dr. Yang Wang. In the third study, kynurenic acid was identified as a potential biomarker of renal tubular 'organic anion transporter (OAT)' channels for predicting kidney injury. Serum kynurenic acid concentrations were dramatically increased in rats treated with an OAT1/3 inhibitor and in OAT1/3 double knockout rats. Further, renal kynurenic acid levels were significantly raised in response to a multidrug resistance-associated protein 4 (MRP4), which is key to drug and toxin excretion. Corresponding author Prof. Xinan Wu speculates by saying, "Our findings could aid in adjusting drug dosage or predicting renal injury via OAT channels." Together, these articles offer hope for improved treatment strategies in the future. Reference Title of original paper: Monoclonal antibody targeting mu-opioid receptor attenuates morphine tolerance via enhancing morphine-induced receptor endocytosis Journal: Journal of Pharmaceutical Analysis DOI: Media Contact: Mengjie Wang +86-(0)29-88960092 [email protected] SOURCE Journal of Pharmaceutical Analysis

Clinical Result

15 Apr 2021

·www.biospace.com

BirchBioMed Welcomes Dr. Jonathan Bourne as New Chief Science Officer

VANCOUVER, BC, April 15, 2021 /PRNewswire/ - BirchBioMed Inc., a clinical-stage immunology company focused on the prevention and reduction of immunological fibrotic conditions and defects in the immune system, is pleased to announce the appointment of translational biophysicist and inventor Jonathan W. Bourne, Ph.D. as its new Chief Science Officer. Dr. Bourne's appointment is in line with BirchBioMed's focus on clinical trials to further drug development and commercialization. "Dr. Bourne's expertise in research, as well as his focus on IP strategy, licensing, and business development, will prove invaluable at this pivotal point in BirchBioMed's development," said Mark S. Miller, BirchBioMed Chairman and CEO. "As Director of Biophysics for Serometrix LLC, Dr. Bourne led the company's biology and biophysics research, successfully patenting methods of allosteric inhibition of PCSK9 for lipid lowering, as well as managing the scientific due diligence for two separate major out-licensing transactions." Dr. Bourne holds eight granted patents, with two others issuing later this year, has co-authored eight published manuscripts and presented eight abstracts at national meetings. Dr. Bourne received his M.S. in Clinical Investigation and his Ph.D. in Physiology, Biophysics and Systems Biology from Cornell University's Weill Graduate School of Medical Sciences in New York. He subsequently completed his postdoctoral training at the Weill Medical College and currently holds an adjunct research faculty appointment at the Hospital for Special Surgery in New York City. Prior to that, Dr. Bourne served as an Adjunct Lecturer in the Department of Biology at the State University of New York College at Geneseo. "Birch BioMed is developing exciting immunomodulatory technologies that have the potential to become life-changing treatments for regenerative medicine. I am honored to join the team to continue advancing these discoveries through clinical development," said Dr. Bourne. About BirchBioMed BirchBioMed, a University of British Columbia (UBC) spinoff, holds the exclusive worldwide pharmaceutical license for two medical therapeutic technologies from UBC that mark significant medical breakthroughs in the treatment of fibrosis and certain autoimmune diseases. In January, BirchBioMed announced positive topline data from its phase 2 trials of FS2 for the treatment of mature keloid scars. The results showed statistically significant improvement versus the market leading scar cream.

100 Deals associated with Kynurenic acid

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Indication	Highest Phase	Country/Location	Organization	Date
Cicatrix	Phase 2	-	BirchBioMed, Inc.Startup	-
Cicatrix	Phase 2	-	University of British Columbia	-

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


SFN2022	Not Applicable	Cognitive Dysfunction	-	kynurenic acid (KMO SNP rs2275163 CC)	mslfaljwzd(arxsbchwhz) = ugmqgzucbl lgvmppndim (whhvenvcrn )	-	14 Nov 2022
SFN2010	Not Applicable	Bipolar Disorder	-	kynurenic acid (Male patients with bipolar disorder)	oxsxfwaflu(twaplpvdqd) = mxtnkpbccp rmbbpofcss (vvjnccjnpf )	-	16 Nov 2010
				kynurenic acid (Female patients with bipolar disorder)	oxsxfwaflu(twaplpvdqd) = ulhzxhulvs rmbbpofcss (vvjnccjnpf )
SFN2007	Not Applicable	Encephalitis, Tick-Borne	-	kynurenic acid (TBE patients)	ixncbnemix(gupcsfmwst) = kjzrqzrufr oskyeaetfo (ukmvohppfy, 1.0)	-	05 Nov 2007
				kynurenic acid (Controls)	ixncbnemix(gupcsfmwst) = cieejvoxat oskyeaetfo (ukmvohppfy, 0.2)
SFN2005	Not Applicable	Schizophrenia	-	kynurenic acid (Schizophrenic patients)	wipnzclmfo(ciwvsblrpq) = ceauhuzzca wfqpkvtjby (mvxbpszwvu, 0.1)	-	14 Nov 2005
				kynurenic acid (Controls)	wipnzclmfo(ciwvsblrpq) = lzjhzzdzhb wfqpkvtjby (mvxbpszwvu, 0.06)
SFN2002	Not Applicable	Ischemia	-	kynurenic acid (Transient global ischemia)	qfjkntjbhs(nqusijcodp) = dcwdeondye bfbkkjmxyy (ubootghdwd ) View more	-	04 Nov 2002
				kynurenic acid (Sham)	qfjkntjbhs(nqusijcodp) = raaotbzxah bfbkkjmxyy (ubootghdwd ) View more

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