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Last update 08 May 2025

VLDLR

Last update 08 May 2025

Basic Info

Synonyms

CARMQ1, CHRMQ1, very low density lipoprotein receptor

+ [5]

Introduction

Multifunctional cell surface receptor that binds VLDL and transports it into cells by endocytosis and therefore plays an important role in energy metabolism. Binds also to a wide range of other molecules including Reelin/RELN or apolipoprotein E/APOE-containing ligands as well as clusterin/CLU (PubMed:24381170, PubMed:30873003). In the off-state of the pathway, forms homooligomers or heterooligomers with LRP8 (PubMed:30873003). Upon binding to ligands, homooligomers are rearranged to higher order receptor clusters that transmit the extracellular RELN signal to intracellular signaling processes by binding to DAB1 (PubMed:30873003). This interaction results in phosphorylation of DAB1 leading to the ultimate cell responses required for the correct positioning of newly generated neurons. Later, mediates a stop signal for migrating neurons, preventing them from entering the marginal zone (By similarity). (Microbial infection) Acts as a receptor for Semliki Forest virus.

Drugs associated with VLDLR

Adenovirus–mediated VLDLR gene transfer therapy(University of Pennsylvania)

Target

VLDLR

Mechanism

VLDLR modulators

Active Org.

University of Pennsylvania

Originator Org.

University of Pennsylvania

Active Indication

Heterozygous familial hypercholesterolemia

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with VLDLR

100 Translational Medicine associated with VLDLR

0 Patents (Medical) associated with VLDLR

6,383

Literatures (Medical) associated with VLDLR

01 Dec 2025·Genes & Nutrition

Changes in triglyceride-rich lipoprotein particle profiles in response to one-week on a low fat or Mediterranean diet by TCF7L2 rs7903146 genotype: a randomized crossover dietary intervention trial

Article

Author: Lai, Chao-Qiang ; Gervis, Julie E ; Parnell, Laurence D ; Ordovas, Jose M ; Lichtenstein, Alice H

AbstractBackgroundThe TCF7L2 gene is a significant genetic factor contributing to the risk of metabolic and cardiovascular diseases (CVD). We previously found that subjects with the TT genotype of TCF7L2 rs7903146 variant, who consume a low-fat diet (LF) had a higher incidence of stroke than subjects with the CC genotype. Yet this association was abolished in subjects with the TT genotype who consumed a Mediterranean-type diet (MetD). However, the mechanism by which MetD diet modulates the association between TCF7L2 and CVD risk is unclear. This study aims to validate these findings under real-world conditions and clinical practice to elucidate the biological mechanisms involved in this correlation.MethodsThirty-five participants with BMI ranging from 27 to 34 kg/m2 were recruited based on rs7903146 genotype. Of those consented to participate, 21 had the CC and 14 had the TT genotype. Participants were randomly assigned to two dietary intervention groups, ensuring an equal distribution of CC and TT carriers. Each participant followed one of two diets (LF or MetD) for one week, followed by a 10-day washout period before switching to the other diet for one week. Blood samples were collected before and after each diet for metabolomic analysis using nuclear magnetic resonance (NMR) spectroscopy. The differential effect of the diets on triglyceride-rich lipoproteins was determined based on TCF7L2 genotype.ResultsThe MetD significantly reduced triglyceride-rich lipoprotein concentrations compared to the LF diet. After consuming the LF diet, TT carriers exhibited more small VLDL particles, potentially contributing to CVD risk compared to CC carriers. However, this difference in risk was not observed with the MetD. Furthermore, the order in which the two diets were crossed affected the triglyceride-rich lipoprotein profile, with LF-MetD regimen showing a stronger effect on triglyceride-rich lipoproteins (TRL) levels than the MetD-LF regimen.ConclusionsOur findings suggest that rs7903146 TT carriers benefit more from a MetD than a LF diet in terms of their triglyceride-rich lipoprotein profile, which may reduce their risk of CVD. These results support the notion that genotype is a factor in determining the extent to which the MetD affects cardiovascular health.

01 May 2025·Poultry Science

Dietary Puerariae Lobatae Radix polysaccharides improve ovarian function and reproductive efficiency in laying hens with fatty liver hemorrhagic syndrome

Article

Author: Ge, Hongfan ; Zhou, Zhenlei ; Zhang, Yanyan ; Ren, Hui ; Wang, Anqi

Fatty liver hemorrhagic syndrome (FLHS) is a common nutritional and metabolic disease in laying hens, leading to a rapid decline in egg production. This study aims to evaluate the antioxidant effects of dietary supplementation with Pueraria Lobatae Radix polysaccharide (PLRP) on laying hens with FLHS induced by a high-energy low-protein (HELP) diet. A total of 72 thirty-seven-wk-old Hy-Line Brown laying hens were divided into 4 groups: basal diet (CON), HELP diet (HELP), HELP + 100 mg/kg PLRP (HELP-Low), and HELP + 300 mg/kg PLRP (HELP-High), with 6 replicates of 3 hens each. After 4 weeks on the HELP diet, PLRP was added to the diet of the HELP-Low and HELP-High groups for 8 weeks. The results demonstrated that PLRP supplementation significantly improved laying rate compared to the HELP group, with the HELP-Low and HELP-High groups exhibiting respective increases of 23.81% and 28.57% (P < 0.01). PLRP also promoted follicular development, increasing the number of stratified, primary, and secondary follicles and improving the ovarian index. Biochemical analysis revealed enhanced antioxidant activity, with increased levels of T-AOC, T-SOD, and GSH-Px and reduced MDA in the liver and ovaries of PLRP-treated hens (P < 0.05). At the molecular level, PLRP upregulated mRNA expression of ER-α, ER-β, MTTP, APOB, APOVLDL-II, and VTG-II in the liver, as well as VLDLR, LHR, and FSHR in the ovaries, facilitating yolk precursor biosynthesis and follicular development (P < 0.05). It indicated that PLRP supplementation mitigates oxidative stress and enhances yolk precursor synthesis, thereby improving egg production in FLHS-affected hens. PLRP shows promise as an effective feed additive for preventing and alleviating FLHS in laying hens. Future studies will investigate the regulatory effects of PLRP on gut microbiota composition and its potential interactions with FLHS in laying hens.

01 May 2025·Journal of Ethnopharmacology

Toxicological evaluation of Artocarpus lacucha ethyl acetate extract: in vitro and in vivo assessment

Article

Author: Ghosh, Nilanjan ; Karmakar, Sanmoy ; Sar, Shuvam ; Banerjee, Tanmoy ; Panda, Parthasarathi ; Mandal, Avishek ; De, Akash ; Sarkar, Arnab ; Halder, Amit Kumar

ETHNOPHARMACOLOGICAL RELEVANCEArtocarpus lacucha Buch. -Ham. (syn. Artocarpus lakoocha) (A. lacucha), is a tropical fruit tree and a member of the Moraceae family. Fruit, bark, foliage, and roots of A. lacucha are broadly utilized in folklore medicine to treat various metabolic and gastrointestinal disorders. The bark of A. lacucha has demonstrated antimicrobial and antinociceptive effects.AIM OF THE STUDYThe study investigated the toxicity of A. lacucha ethyl acetate bark extract (AL-EAE) employing both in vitro and in vivomodels.MATERIALS AND METHODSAL-EAE was extracted by soxhlation of powdered bark. The phytochemical fingerprint of AL-EAE was established employing LC-MS technique. The presence of heavy metals was determined by atomic absorption spectroscopy (AAS). Cytotoxicity of AL-EAE (3.9-250 μg/mL) was evaluated by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay in human embryonic kidney cells (HEK293). The acute oral toxicity of AL-EAE was ascertained by administering 500, 1000, and 2000 mg/kg B.W. doses in rats of both sexes. Rats were treated with AL-EAE orally at 200, 400, and 600 mg/kg B.W. doses on a daily basis for 28 days in order to evaluate subacute toxicity. Clinical and toxicological parameters were noted after every 24 h. After the course of treatment, the safety of AL-EAE was evaluated by investigating various biochemical, haematological, and histopathological markers.RESULTSLC-MS analysis indicates the presence of phenols and flavonoids in A. lacucha bark extracts. AAS analysis revealed the safety limits of heavy metals in AL-EAE as recommended by ICH. AL-EAE was not found cytotoxic in HEK293 cells (IC₅₀ more than 250 μg/mL). No adverse clinical syndromes or mortality were observed in the acute toxicity study. The alterations in body weight (B.W.) and relative organ weights (ROWs) were found to be non-significant. In the sub-acute toxicity assessment, changes in food intake and mild diarrhoea were observed at 600 mg/kg/day B.W. Changes in ROWs at 600 mg/kg/day and B.W. at 400 and 600 mg/kg/day dose were observed. However, significant alterations in biochemical (TG, VLDL, AST, and ALP) and haematological (haemoglobin, MCHC, eosinophils, monocyte) parameters were observed at 400 and 600 mg/kg/day B.W. doses. Histopathological studies illustrated significant inflammation in the liver, pancreas, and spleen at 600 mg/kg/day B.W. doses.CONCLUSIONThe findings demonstrated that AL-EAE did not possess cytotoxicity in vitro. In both acute and subacute toxicity studies, AL-EAE was shown to be nontoxic, where 400 mg/kg/day was the no-observed-adverse-effect level (NOAEL) dosage in rodents.

News (Medical) associated with VLDLR

26 Apr 2023

·www.globenewswire.com

Ashvattha Therapeutics Presents Preclinical Data on anti-VEGF Nanomedicine D-4517.2 at the 2023 ARVO Annual Meeting

Data demonstrated that a single oral dose of D-4517.2 significantly reduced choroidal neovascularization (CNV) lesions to a level comparable to D-4517.2 delivered subcutaneously and Aflibercept administered intravitreally at the same mass dose in a laser-induced CNV mouse modelFindings from a second preclinical study in a VLDLR−/− mouse model demonstrated oral and subcutaneous administration of D-4517.2 reduces CNV lesions by targeting activated microglia and macrophages in the choroid and retinaThese preclinical data support the development of D-4517.2 as an oral treatment for neovascular age-related macular degeneration (wet AMD) and diabetic macular edema (DME) with the potential to eliminate burdensome intravitreal injections for patients REDWOOD CITY, Calif., April 26, 2023 (GLOBE NEWSWIRE) -- Ashvattha Therapeutics (“Ashvattha”), a clinical-stage company advancing a new class of nanomedicine therapeutics that transverse tissue barriers to selectively target activated cells in regions of inflammation, today announced two preclinical data sets demonstrating the efficacy of its anti-angiogenic precision nanomedicine, D-4517.2. The data were shared in an oral presentation and poster at the Association for Research in Vision and Ophthalmology (ARVO) annual meeting held on April 23-27, 2023 in New Orleans, LA. D-4517.2 is a novel precision nanomedicine that inhibits neovascularization by targeting activated microglia and hypertrophic retinal pigment cells, cells responsible for the increased vascularization associated with neovascular age-related macular degeneration (wet AMD) and diabetic macular edema (DME). “Patients suffering from wet AMD and DME often have to endure injections directly into the eye at a specialist’s office in order to find any relief. This data supports the development of an oral formulation of D-4517.2 as an alternative to injections while greatly reducing the treatment burden on patients,” said Jeff Cleland, CEO, co-founder, and chairman of Ashvattha Therapeutics. “The preclinical data also builds on previous findings that demonstrate our precision nanomedicines selectively target regions of inflammation at a cellular level and cross biological barriers including the blood-retinal barrier.” Natacha Le Moan, Ph.D, Head of Translational Sciences at Ashvattha gave an oral presentation titled “Oral Formulation Development of the Anti-Angiogenesis Drug D-4517.2 to Treat Age-related Macular Degeneration (wet AMD) and Diabetic Macular Edema (DME)” in which she discussed the efficacy of the oral formulation of D-4517.2 in a mouse model of wet AMD. Key highlights from presentation: Results indicated that a single subcutaneous dose of D-4517.2 (40 mg) significantly reduces CNV lesion area by~2-fold compared to vehicle control, which is consistent with previous observations and comparable with aflibercept efficacy.A single oral dose of D-4517.2 (40 mg) also significantly reduces CNV lesion area and vascular leakage by ~2-fold. A 200 mg oral dose further reduces the CNV lesion area by ~3.5 fold.These results suggest that oral administration of D-4517.2 has similar efficacy to aflibercept, and similar bioavailability when given orally or subcutaneously. This study supports the development of D-4517.2 as a potentially safe and effective oral agent for patients suffering from wet AMD or DME. Elia Duh, a collaborator from Johns Hopkins University presented a poster titled “Suppression of subretinal neovascularization in Vldlr knockout mice by systemic administration of a targeted VEGF-receptor inhibitor,” in which he discussed the cellular localization and efficacy of D-4517.2 in a wet AMD mouse model. Key highlights from poster presentation: The study evaluated the localization of D-4517.2 in Vldr -/- knockout mice, an animal model with symptoms of type III wet AMD after birth.Results indicated the nanomedicine conjugated with a fluorophore (D-Cy5) colocalized with activated microglia and macrophages within regions of ocular inflammation in Vldr-/- mice.Oral and subcutaneous administration of D-4517.2 significantly reduces the number of CNV lesions in Vldlr-/- mice suggesting a benefit of selectively inhibiting VEGFR in activated microglia/macrophages and RPE cells in the retina and choroid. The data further support that systemic administration of D-4517.2 is effective in reducing neovascular lesions associated with AMD and selectively targets activated microglia and macrophages. About Wet AMD and DME Wet age-related macular degeneration (wet AMD) is a retinal disease that develops when abnormal blood vessels grow into the macula – a part of the retina at the back of the eye which is responsible for sharp central vision. These vessels leak blood or fluid which can lead to rapid loss of central vision. Wet AMD can be treated if caught early with drugs to stop the growth of the abnormal vessels. According to the World Health Organization, 196 million people have AMD globally, including 10.4 million people with moderate to severe vision impairment or blindness. Diabetic macular edema (DME) is a retinal disease that develops when there is an accumulation of fluid in the macula due to leaking blood vessels. DME is a result of diabetic retinopathy, a disease that damages the blood vessels in the retina which if left untreated builds pressure in the eye and leaks fluid. A recent study estimated approximately 100 million individuals suffer from DME globally.1 About D-4517.2  D-4517.2 is a potent anti-angiogenic nanomedicine that crosses the blood-retinal barrier and selectively targets activated microglia, macrophages and hypertrophic retinal pigment epithelial cells in the eye. D-4517.2 has the potential to change the current treatment paradigm for neovascular age-related macular degeneration (wet AMD) and diabetic macular edema (DME) by offering an at-home dosing option by a subcutaneous route of administration rather than delivery via intravitreal injection (injection into the eye). D-4517.2 is in a Phase 2 clinical trial in patients with wet AMD or DME. About Ashvattha Therapeutics Ashvattha Therapeutics is advancing a new class of clinical-stage nanomedicine therapeutics that transverse tissue barriers to selectively target activated cells only in regions of inflammation. Our targeted nanomedicine approach seeks to redefine precision medicine, empowering a new standard of care across ophthalmology, neurology, and inflammation. For more information, visit: www.avttx.com 1. Duphare C, Desai K, Gupta P, et al. Diabetic Macular Edema. [Updated 2023 Mar 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554384/ Media Contact Sky Striar LifeSci Communications 617-797-6672 sstriar@lifescicomms.com

Clinical ResultPhase 2

03 Apr 2023

·www.biospace.com

Ashvattha Therapeutics to Present Preclinical Data at the AACR and ARVO 2023 Annual Meetings

Preclinical data to be presented at AACR will showcase the potential effect of D-4559, a potent macrophage switching nanomedicine, on reducing tumor growth in a mouse model of hepatocellular carcinoma, a type of liver cancer Ashvattha will present preclinical data at ARVO on its oral formulation of D-4517.2, a potent anti-angiogenic nanomedicine, in a laser-induced choroidal neovascularization (CNV) mouse model, and compare its efficacy with intravitreal aflibercept Collaborators from John Hopkins University will also present preclinical data at ARVO on the effect of D-4517.2 systemically administered in a mouse genetic model of subretinal vascular disease REDWOOD CITY, Calif., April 03, 2023 (GLOBE NEWSWIRE) -- Ashvattha Therapeutics (“Ashvattha”), a clinical-stage company developing a new class of nanomedicines, today announced that the company will present preclinical data at the upcoming American Association for Cancer Research (AACR) and the Association for Research in Vision and Ophthalmology (ARVO) 2023 annual meetings. The presentations will showcase the potential of Ashvattha’s pipeline of nanomedicines to transverse tissue barriers to selectively target activated cells in regions of inflammation. The poster presented at AACR will be published in an online-only Proceedings supplement to the AACR journal Cancer Research on Friday, April 14. Details for the presentations are as follows: AACR Annual Meeting 2023 April 14 – 19, 2023 Orange County Convention Center, Orlando, Florida Poster Title: A potent macrophage switching drug D-4559 reduces tumor growth in a hepatocellular carcinoma mouse model Session Title: Late-Breaking Research: Immunology 2 Abstract Presentation Number: LB208 Presenter: Naze Avci, Ph.D., Ashvattha Therapeutics Date/Time: Tuesday, April 18, 2023, 9:00 a.m. – 12:30 p.m. ET Location: Poster Section 36 ARVO 2023 Annual Meeting April 23 – 27, 2023 The New Orleans Ernest N. Morial Convention Center, New Orleans, Louisiana Title: Oral Formulation Development of the Anti-Angiogenesis Drug D-4517.2 to Treat Age-related Macular Degeneration (wet-AMD) and Diabetic Macular Edema (DME) Session Title: AMD: New drugs, delivery systems and mechanisms of action 2 Presenter: Natacha Le Moan, Ph.D., Ashvattha Therapeutics Session Number: 204 Date/Time: Monday, April 24, 2023, 12:45 p.m. - 1:00 p.m. CT Location: Room R01 Title: Suppression of subretinal neovascularization in Vldlr knockout mice by systemic administration of a targeted VEGF-receptor inhibitor Session Title: Cellular pathways underlying retinal degeneration Presenter: Elia Duh, M.D., Johns Hopkins University School of Medicine Session Number: 415 Poster Presentation Number: 3900-B0180 Date/Time: Wednesday, April 26, 2023, 10:30 a.m. – 12:30 p.m. CT Location: Exhibit Hall – B About Ashvattha Therapeutics Ashvattha Therapeutics is advancing a new class of clinical-stage nanomedicine therapeutics that transverse tissue barriers to selectively target activated cells only in regions of inflammation. Our targeted nanomedicine approach seeks to redefine precision medicine, empowering a new standard of care across ophthalmology, neurology, and inflammation. For more information, visit: Media Contact Sky Striar LifeSci Communications 617-797-6672 sstriar@lifescicomms.com

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VLDLR

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