Last update 21 Mar 2024

RPS6KB1

Ribosomal protein S6 kinase beta-1

Last update 21 Mar 2024

Basic Info

Synonyms

70 kDa ribosomal protein S6 kinase 1, p70 ribosomal S6 kinase alpha, p70 S6 kinase alpha

+ [16]

Introduction

Serine/threonine-protein kinase that acts downstream of mTOR signaling in response to growth factors and nutrients to promote cell proliferation, cell growth and cell cycle progression. Regulates protein synthesis through phosphorylation of EIF4B, RPS6 and EEF2K, and contributes to cell survival by repressing the pro-apoptotic function of BAD. Under conditions of nutrient depletion, the inactive form associates with the EIF3 translation initiation complex. Upon mitogenic stimulation, phosphorylation by the mammalian target of rapamycin complex 1 (mTORC1) leads to dissociation from the EIF3 complex and activation. The active form then phosphorylates and activates several substrates in the pre-initiation complex, including the EIF2B complex and the cap-binding complex component EIF4B. Also controls translation initiation by phosphorylating a negative regulator of EIF4A, PDCD4, targeting it for ubiquitination and subsequent proteolysis. Promotes initiation of the pioneer round of protein synthesis by phosphorylating POLDIP3/SKAR. In response to IGF1, activates translation elongation by phosphorylating EEF2 kinase (EEF2K), which leads to its inhibition and thus activation of EEF2. Also plays a role in feedback regulation of mTORC2 by mTORC1 by phosphorylating RICTOR, resulting in the inhibition of mTORC2 and AKT1 signaling. Mediates cell survival by phosphorylating the pro-apoptotic protein BAD and suppressing its pro-apoptotic function. Phosphorylates mitochondrial URI1 leading to dissociation of a URI1-PPP1CC complex. The free mitochondrial PPP1CC can then dephosphorylate RPS6KB1 at Thr-412, which is proposed to be a negative feedback mechanism for the RPS6KB1 anti-apoptotic function. Mediates TNF-alpha-induced insulin resistance by phosphorylating IRS1 at multiple serine residues, resulting in accelerated degradation of IRS1. In cells lacking functional TSC1-2 complex, constitutively phosphorylates and inhibits GSK3B. May be involved in cytoskeletal rearrangement through binding to neurabin. Phosphorylates and activates the pyrimidine biosynthesis enzyme CAD, downstream of MTOR (PubMed:11500364, PubMed:12801526, PubMed:14673156, PubMed:15071500, PubMed:15341740, PubMed:16286006, PubMed:17052453, PubMed:17053147, PubMed:17936702, PubMed:18952604, PubMed:19085255, PubMed:19720745, PubMed:19935711, PubMed:19995915, PubMed:23429703). Following activation by mTORC1, phosphorylates EPRS and thereby plays a key role in fatty acid uptake by adipocytes and also most probably in interferon-gamma-induced translation inhibition (PubMed:28178239).

Drugs associated with RPS6KB1

Oleandrin

Target

AP-1 x FGFs x FLI1 x NF-κB x Na/K-ATPase x RPS6KB1 x mTOR

Mechanism

AP-1 inhibitors [+7]

Active Org.

U.S. Army Medical Research Institute for Infectious Diseases [+2]

Originator Org.

U.S. Army Medical Research Institute for Infectious Diseases

Active Indication

Pancreatic Cancer [+1]

Inactive Indication

Advanced cancer [+6]

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

EPGN-1370

Target

RPS6KB1

Mechanism

RPS6KB1 inhibitors

Active Org.

Epigen Biosciences, Inc.

Originator Org.

Epigen Biosciences, Inc.

Active Indication

Fragile X Syndrome

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

RJ-28

Target

RPS6KB1

Mechanism

RPS6KB1 inhibitors

Active Org.

Xavier University of Louisiana

Originator Org.

Xavier University of Louisiana

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with RPS6KB1

NCT02329717 / Unknown statusPhase 2

A Phase II, Single-arm, Open-label, Bayesian Adaptive Efficacy and Safety Study of PBI-05204 in Patients With Stage IV Metastatic Pancreatic Adenocarcinoma

This study evaluates the efficacy and safety of PBI-05204, an extract of the leaves of Nerium oleander, in patients with Stage IV metastatic pancreatic cancer. All patients will receive PBI-05204.

Start Date01 Apr 2015

Sponsor / Collaborator

Phoenix Biotechnology, Inc.

NCT01562301 / WithdrawnPhase 1IIT

A Phase I Study of the Combination of Carboplatin, Docetaxel, and Increasing Doses of Sublingual Anvirzel (Nerium Oleander) in Advance Non-Small Cell Lung Cancer

The goal of this clinical research study is to find the highest tolerable dose of Anvirzel (Nerium Oleander) that can be given to lung cancer patients receiving standard therapy with carboplatin and docetaxel. Researchers also want to learn what effect Nerium Oleander may have in combination with carboplatin and docetaxel.

Start Date01 Jun 2014

Sponsor / Collaborator

The University of Texas MD Anderson Cancer Center

[+2]

NCT01971515 / CompletedPhase 1

A Phase I, First-in-Human, Dose Escalation Trial of MSC2363318A, a Dual p70S6K/Akt Inhibitor, in Subjects With Advanced Malignancies

This is a Phase 1, first-in-human, open-label, non-randomized, dose escalation, trial to explore the safety, tolerability, pharmacokinetic (PK), pharmacodynamic (PD) and clinical activity signals of MSC2363318A.

Start Date13 Dec 2013

Sponsor / Collaborator

EMD Serono, Inc.

100 Clinical Results associated with RPS6KB1

100 Translational Medicine associated with RPS6KB1

0 Patents (Medical) associated with RPS6KB1

3,847

Literatures (Medical) associated with RPS6KB1

01 Apr 2024·Oncology letters

Rapamycin inhibits B16 melanoma cell viability invitro and invivo by inducing autophagy and inhibiting the mTOR/p70‑S6k pathway.

Article

Author: Penghui Wang ; Haifang Zhang ; Kaikai Guo ; Chun Liu ; Shimin Chen ; Baopeng Pu ; Sirun Chen ; Tong Feng ; Hanyi Jiao ; Chang Gao

Rapamycin is an immunosuppressant that has been shown to prevent tumor growth following organ transplantation. However, its exact mode of antitumor action remains unknown. The present study used the B16-F10 (B16) murine melanoma model to explore the antitumor mechanism of rapamycin, and it was revealed that rapamycin reduced B16 cell viability in vitro and in vivo. In addition, in vitro and in vivo, the results of western blotting showed that rapamycin reduced Bcl2 expression, and enhanced the protein expression levels of cleaved caspase 3 and Bax, indicating that it can induce the apoptosis of B16 melanoma cells. Furthermore, the results of cell cycle analysis and western blotting showed that rapamycin induced B16 cell cycle arrest in the G₁ phase, based on the reduction in the protein expression levels of CDK1, cyclin D1 and CDK4, as well as the increase in the percentage of cells in G₁ phase. Rapamycin also significantly increased the number of autophagosomes in B16 melanoma cells, as determined by transmission electron microscopy. Furthermore, the results of RT-qPCR and western blotting showed that rapamycin upregulated the protein expression levels of microtubule-associated protein light chain 3 (LC3) and Beclin-1, while downregulating the expression of p62 in vitro and in vivo, thus indicating that rapamycin could trigger cellular autophagy. The present study revealed that rapamycin in combination with chloroquine (CQ) further increased LC3 expression compared with that in the CQ group, suggesting that rapamycin induced an increase in autophagy in B16 cells. Furthermore, the results of western blotting showed that rapamycin blocked the phosphorylation of p70 ribosomal S6 kinase (p70-S6k) and mammalian target of rapamycin (mTOR) proteins in vitro and in vivo, thus suggesting that rapamycin may exert its antitumor effect by inhibiting the phosphorylation of the mTOR/p70-S6k pathway. In conclusion, rapamycin may inhibit tumor growth by inducing cellular G₁ phase arrest and apoptosis. In addition, rapamycin may exert its antitumor effects by inducing the autophagy of B16 melanoma cells in vitro and in vivo, and the mTOR/p70-S6k signaling pathway may be involved in this process.

01 Mar 2024·Animal nutrition (Zhongguo xu mu shou yi xue hui)

Leucine regulates lipid metabolism in adipose tissue through adipokine-mTOR-SIRT1 signaling pathway and bile acid-microbe axis in a finishing pig model.

Article

Author: Yunju Yin ; Saiming Gong ; Mengmeng Han ; Jingzun Wang ; Hanjing Shi ; Xianji Jiang ; Liu Guo ; Yehui Duan ; Qiuping Guo ; Qinghua Chen ; Fengna Li

This study was conducted to explore the regulatory mechanism of leucine (Leu) on lipid metabolism of finishing pigs. Twenty-four Duroc × Landrace × Large cross pigs with an average body weight of 68.33 ± 0.97 kg were randomly allocated into 3 treatment groups with 8 replicates per group (1 pig per replicate). The dietary treatments were as follows: control group (CON), 0.25% Leu group and 0.50% Leu group. The experimental period was 42 d. The results showed as follows. (1) Compared with the CON, 0.25% and 0.50% Leu increased (P < 0.01) the average daily gain (ADG), while the average backfat thickness (ABT) and the ratio of feed intake to body weight gain (F:G ratio) were decreased (P < 0.05). (2) In the 0.25% Leu group, the relative mRNA expression levels of sterol regulatory element binding protein-1c (SREBP1c), recombinant fatty acid transport protein 1 (FATP1), chemerin and peroxisome proliferator-activated receptor γ (PPARγ) were decreased but the level of fatty acid binding protein 4 (FABP4) and fatty acid translocase (FAT/CD36) were increased in backfat tissue. In the 0.25% Leu group, the protein levels of p-Rictor, p-Raptor, p-eIF4E-binding protein 1 (p-4EBP1), p-silent mating type information regulator 2 homolog 1 (p-SIRT1) and acetylation ribosome s6 protein kinase 1 (Ac-S6K1) were increased (P < 0.05). (3) Compared to the CON, the diversity of gut microbiota in the 0.25% Leu group was increased. Principal component analysis showed that the relative abundance of Bacteroidetes, Lactobacillus and Desulfovibrio was higher in the 0.25% Leu group than the CON, but the relative abundance of Firmicutes, Treponema and Shigella was lower than in the CON (P < 0.05). (4) Four different metabolites were screened out from the serum of finishing pigs including allolithocholic acid (alloLCA), isolithocholic acid (isoLCA), ursodeoxycholic acid (UDCA) and hyodeoxycholic acid (HDCA), which correlate to various degrees with the above microorganisms. In conclusion, Leu could promote adipose tissue lipolysis of finishing pigs through the mTOR-SIRT1 signaling pathway, and S6K1 is acetylated at the same time, and the interaction between gut microbiota and bile acid metabolism is also involved.

01 Mar 2024·Animal nutrition (Zhongguo xu mu shou yi xue hui)

Hexokinase 1 and 2 mediates glucose utilization to regulate the synthesis of kappa casein via ribosome protein subunit 6 kinase 1 in bovine mammary epithelial cells.

Article

Author: Tianyu Yang ; Jia Guo ; Han Song ; Osmond Datsomor ; Yuhang Chen ; Maocheng Jiang ; Kang Zhan ; Guoqi Zhao

Glucose plays a vital part in milk protein synthesis through the mTOR signaling pathway in bovine mammary epithelial cells (BMEC). The objectives of this study were to determine how glucose affects hexokinase (HK) activity in BMEC and investigate the regulatory effect of HK in kappa casein (CSN3) synthesis via the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway in BMEC. For this, HK1 and HK2 were knocked out in BMEC using the CRISPR/Cas9 system. The gene and protein expression, glucose uptake, and cell proliferation were measured. We found that glucose uptake, cell proliferation, CSN3 gene expression levels, and expression of HK1 and HK2 increased with increasing glucose concentrations. Notably, glucose uptake was significantly reduced in HK2 knockout (HK2KO) BMEC treated with 17.5 mM glucose. Moreover, under the same glucose treatment conditions, the proliferative ability and abundance of CSN3 were significantly diminished in both HK1 knockout (HK1KO) and HK2KO BMEC compared with that in wild-type BEMC. We further observed that the phosphorylation levels of ribosome protein subunit 6 kinase 1 (S6K1) were reduced in HK1KO and HK2KO BMEC following treatment with 17.5 mM glucose. As expected, the levels of glucose-6-phosphate and the mRNA expression levels of glycolysis-related genes were decreased in both HK1KO and HK2KO BMEC following glucose treatment. These results indicated that the knockout of HK1 and HK2 inhibited cell proliferation and CSN3 expression in BMEC under glucose treatment, which may be associated with the inactivation of the S6K1 and inhibition of glycolysis.

News (Medical) associated with RPS6KB1

28 Feb 2024

·www.prnewswire.com

PharmAust announces positive Phase 1 MEND Study Top-Line Results in MND / ALS

Highlights: Monepantel displays a superior safety, tolerability to the leading FDA approved drug Relyvrio® Preliminary efficacy data shows a 58% reduction in the rate of disease progression for Cohort 2 (High Dose) using the FDA primary efficacy endpoint, ALSFRS-R Confirmation that monepantel and its active metabolite, monepantel sulfone, are both detected in cerebrospinal fluid Optimal dose identified for the pivotal Phase 2/3 clinical study, due to commence in Q3 CY2024 PERTH, Australia, Feb. 28, 2024 /PRNewswire/ -- PharmAust Limited (ASX: PAA & PAAOA) ("PharmAust" or "the Company"), a clinical-stage biotechnology company, is pleased to announce that it has met its primary safety and tolerability endpoints with monepantel (MPL) and, importantly, demonstrated a positive signal of potential efficacy. Rates of disease progression in patients with Motor Neurone Disease (MND) / Amyotrophic Lateral Sclerosis (ALS) measured by changes in ALSFRS-R may be slowed by 58% for Cohort 2, when compared to an external control cohort (PRO-ACT database). Study Design The Phase 1 MEND Study was a multicentre, open label study comprising a 24-hour escalating single-dose PK study and 4-week repeated escalating dose study to establish the safety, tolerability and pharmacokinetic (PK) parameters of MPL administered orally to patients with MND/ALS. Twelve participants were enrolled in cohorts of 6 patients across 2 sites. Cohort 1 was administered 2 and 6 mg/kg/day dose levels, and Cohort 2 was administered 4 and 10 mg/kg/day dose levels. Participants continued to receive MPL treatment until they were offered dose escalation or until the end of treatment. Safety and Tolerability Endpoints The safety and tolerability profile of MPL included no treatment‑related deaths, with all 12 patients successfully completing the study, and no dose limiting toxicities experienced. A total of 56 treatment‑emergent Adverse Events (AEs) were reported. Only 3 AEs, graded mild, were considered possibly related to the study drug. Patients have remained on daily treatment of MPL for 10 to 16 months. Upon completing the study, all participants continued receiving MPL via a special access scheme and opted to enrol on a 12-month open-label extension (OLE) study. Exploratory Efficacy Endpoints The study's exploratory clinical efficacy markers included the ALS Functional Rating Scale-Revised ("ALSFRS-R"), ALSSQOL-R Quality of Life Questionnaire, Edinburgh Cognitive and Behavioural ALS Screen ("ECAS") and Slow Vital Capacity ("SVC"), a measure of respiratory function. ALSFRS-R is the accepted FDA primary efficacy measure to determine ALS disease progression. It assesses for changes in a person's physical abilities over time of 12 specific functions including speech, walking, climbing stairs, dressing/hygiene, handwriting, turning in bed, cutting food, salivation, swallowing and breathing. There were no significant differences in ALSFRS-R scores between pre-dose and end of treatment for all 12 patients (p=0.78), Cohort 1 (p=0.41), and Cohort 2 (p=0.88) suggesting that treatment with monepantel over 8 – 12 months slowed the rate of disease progression. A more thorough comparative analysis of the rate of decline in ALSFRS-R scores performed by Berry Consultants against 30 matched controls from the PRO-ACT database for ALSFRS-R decline has highlighted the potential for MPL to tackle disease burden and slow disease progression. The PRO-ACT database is the largest publicly available repository of merged ALS clinical study data. Clinical study data were pooled from 16 completed Phase 2/3 ALS/MND clinical studies and one observational study. Over 8 million de-identified longitudinally collected data points from more than 8,600 persons with ALS were standardised across studies and merged to create the PRO-ACT database. This database includes demographics, family histories, and longitudinal clinical and laboratory data. Matching is a procedure that finds treatment and control subjects with similar baseline characteristics to enable treatment effect estimation. For all 12 patients, the estimated rate of decline was -0.74 (p=0.08) in ALSFRS-R points per month or a 39% slowing in ALSFRS-R decline. For Cohort 1 the estimated rate of decline was -0.83 (p=0.40) in ALSFRS-R points per month or a 23% slowing in ALSFRS-R decline. For Cohort 2 the estimated rate of decline was -0.60 (p=0.11) in ALSFRS-R points per month or a 58% slowing in ALSFRS-R decline indicating a dose response. Using the prognostic predictor model described in Elamin et al., 2015, [1]depending on the current severity of the disease, a 0.48 slope change as calculated for all 12 patients could provide patients with an additional 13.5- 56.5 months in median survival. Currently approved treatments for ALS/MND provide approximately 2 – 9 months in additional life expectancy. * Berry Consultants analysis. ** Duration is dependent upon disease severity at baseline. The results of the additional exploratory efficacy measures of ALSSQOL-R (p=0.11), ECAS (p=0.21), and SVC (p=0.93) further supported slowing in disease progression. In addition, the analysis of biomarkers provided supplemental supporting evidence that MPL slows disease progression with a large reduction in cerebrospinal fluid neurofilament light chain (NfL), which is a measure of neuronal damage, amongst consenting patients (n=3). Pharmacokinetics Concentrations of MPL sulfone, the active metabolite of MPL, increased proportionally with the higher doses of MPL. MPLS was found in the cerebrospinal fluid indicating that both MPL and MPLS have the ability to cross the blood brain barrier. Target Engagement (mTOR Pathway) Target engagement of the mTOR pathway (p-EIF4EBP1 and p-RPS6KB1) in the peripheral mononuclear blood cells was confirmed at all dose levels. MEND participant, S-W, commented: "The Monepantel phase 1 study has been a very positive experience for me with no ill effects at all. At Calvary I have been treated with the most kind, caring and considerate doctors, nursing & administration staff and I know I am receiving the best care possible. I am more than happy to participate in this trial with the knowledge that MND patients may be helped in the future." MEND participant, L-G, commented: "I feel that the Monepantel may have slowed my neurological deterioration. Increasing dosage from 3 per day to 4 may also have been beneficial. My dosage was increased to 6 several days ago. There appears to be no side effects with it." Associate Professor Susan Mathers commented: "This study has shown oral Monepantel to be safe and well tolerated by people with MND. Given the promising findings on preliminary efficacy markers, I look forward to progressing a phase 2 study as soon as possible" PharmAust Chief Executive Officer Dr Michael Thurn commented: "The release of the top-line Phase 1 MEND study results is an exciting milestone for PharmAust as we take a significant step towards helping people diagnosed with this rare and incurable disease. The 58% slowing in ALSFRS-R decline amongst Cohort 2 participants clearly demonstrates the potential to provide meaningful clinical benefit to people living with MND/ALS. To know that we have potentially prolonged the lives of 12 patients is extremely satisfying and humbling. We now look forward to advancing discussions with strategic partners who share our vision for monepantel. I want to thank the trial participants, their caregivers, and families, as well as the sites' principal investigators, Associate Professor Susan Mathers and Professor Dominic Rowe, and their study coordinators for their tremendous ongoing contribution to the MEND study." PharmAust acknowledges the support of FightMND and its donors, in particular the patients, their families and friends and their support network. About FightMND Founded in 2014, FightMND was established in Australia with the purpose of finding effective treatments and ultimately a cure for Motor Neuron Disease (MND), also referred to as ALS or Lou Gehrig's Disease. FightMND, with its vision of a world without MND, is one of the largest independent funders of MND research in the world. Since 2014, FightMND has investment more than $98 million into MND research and care equipment to improve the lives of those fighting the disease. FightMND is determined to help facilitate the translation of the growing body of new knowledge about the disease into a cure for MND patients in Australia and abroad. For more information about FightMND, visit the website at About Berry Consultants Berry Consultants is a statistical consulting company based in Austin, Texas USA, specialising in innovative clinical trial design, analysis, execution, and software solutions for the pharmaceutical and medical device industry. Berry Consultants employs world-renowned experts in Bayesian statistics and strives to set the standard for adaptive clinical trial design and analysis across all medical disciplines. The Board authorises this announcement. Enquiries: Dr Michael Thurn Chief Executive Officer [email protected] Media: Matthew Wright NWR Communications [email protected] 0451 896 420 P +61 (8) 9202 6814 F +61 (8) 9467 6111 About PharmAust Limited: PharmAust Limited is listed on the Australian Securities Exchange (ASX Code: PAA). PAA is a clinical-stage biotechnology company developing therapeutics for human and animal health applications. The company is focused on repurposing monepantel (MPL) for human neurodegenerative diseases and treating cancer in dogs. MPL is a potent and safe inhibitor of the mTOR pathway. This pathway plays a central role in cell growth and proliferation of cancer cells and degenerating neurons. The mTOR pathway regulates the cellular "cleaning process", where toxic protein is broken down into macromolecules to be reused. This autophagic process is disrupted in most neurodegenerative diseases, including motor neurone disease (MND/ALS). PAA's lead MPL program is for the treatment of MND/ALS, a rare, incurable disease. The company is currently completing a Phase 1 study in patients with MND/ALS. Top-line results are expected to be announced in Q1 CY2024. PAA anticipates starting an adaptive Phase 2/3 clinical study in H2 CY 2024 that could lead to accelerated approval with the US Food and Drug Administration in 2026. PAA is preparing to start a pivotal field trial in dogs with B-Cell Lymphoma to enable product registration in the US in 2025. PAA has previously successfully completed a Phase 1 oncology clinical study of monepantel in humans and pilot studies in canine cancer. SOURCE PharmAust Limited

Phase 1Clinical ResultPhase 2

04 Jan 2024

·www.globenewswire.com

Evexta Bio Announces the Appointment of Paul Gineste, PharmD, as Chief Development Officer

Evexta Bio Announces the Appointment of Paul Gineste, PharmD, as Chief Development Officer Paul Gineste brings 25 years of experience in clinical development and strategy with leading international pharmaceutical and biotech companies.Recently, Paul served as Vice President, Clinical Operations at Abivax, where he led the development of drug candidates from discovery through global Phase 3 programs. Paris, France, January 4, 2024 - Evexta Bio SA, a clinical-stage biotechnology company focused on developing first-in-class therapies in oncology, announces the appointment of Paul Gineste as Chief Development Officer (CDO), effective January 1, 2024. Paul is an experienced senior executive with a track record of successful achievements in the Pharma and Biotech Industry. He has worked with leading international pharmaceutical and biotech companies, including as International Clinical Trials Manager at Boehringer Ingelheim, Head of Clinical Research and Development at Altana Pharma, Executive Vice President, Clinical Development at Theravectys, a lentiviral vector spin-off from the Institut Pasteur, and most recently for 9 years as Vice President, Clinical Operations at Abivax, where he led drug candidates from discovery through global Phase 3 programs. Scott Filosi, CEO of Evexta Bio, said: "I am delighted to welcome Paul as the new Chief Development Officer of Evexta Bio. With his extensive track record in the pharmaceutical and biotech industries, Paul is the best suited to lead our clinical development and strategy as our lead candidate, rupitasertib, is expected to enter a phase 2/3 clinical trial in refractory ER+ HER2 metastatic breast cancer.” Paul Gineste, PharmD, CDO of Evexta Bio, added: “I am genuinely pleased to join Evexta Bio and its experienced management team to advance its development strategy and in particular its clinical programs. Evexta Bio has two proprietary therapeutic assets with original mechanisms of action that may address unmet medical needs in multiple cancer indications. I look forward to leading and accelerating their clinical development.” ***** Upcoming opportunity to meet our team: EVEXTA BIO will be in San Francisco, CA, during the JP Morgan's 42nd Annual Healthcare Conference, January 8-11, 2024. Contact us today to arrange a meeting with our executives in San Francisco: Scott Filosi, Chief Executive Officer, and Dominique Bridon, Chief Scientific Officer. About Evexta Bio (https://www.evextabio.com) Evexta Bio, formerly Diaccurate, is a biopharmaceutical company revolutionizing cancer treatment with potential first-in-class therapies with unique mechanisms of action for combating tumor resistance . Now in the clinic, the French biotech is currently developing two proprietary therapeutic assets across several indications: Rupitasertib, formerly DIACC3010, a first-in-class S6K inhibitor addressing tumor resistance while blocking the compensatory AKT feedback loop. The oral anti-tumor agent is expected to enter phase 2/3 clinical trial in refractory ER+ HER2- metastatic breast cancer. EVX-020, formerly DIACC2020, an antibody-drug conjugate program using a first-in-class KIF20A kinesin inhibitor as payload in hematological and solid tumors. Founded by Truffle Capital, Evexta Bio has forged alliances with leaders in academia and industry, including CNRS, Paoli-Calmettes Institute (Marseille, France) and Merck KGaA (Darmstadt, Germany). The company is supported by seasoned management team, board of directors and medical advisory board. Contacts ATCG PARTNERSMarie Puvieux+33 (0)6 10 54 36 72presse@atcg-partners.com Attachment PR in English

Executive Change

06 Nov 2023

·www.biospace.com

Diaccurate Announces the Appointment of Scott Filosi as CEO and Corporate Name Change to Evexta Bio

Diaccurate Announces the Appointment of Scott Filosi as EVEXTA BIOCEO and Corporate Name Change to Evexta Bio Scott Filosi brings more than 30 years of experience in market access and commercialization of innovative medicines at a global level. New name reflects the company's focus on its innovative portfolio of drug candidates that push the boundaries of precision oncology. Paris, France, November 6, 2023 - Diaccurate SA, a clinical-stage biotechnology company focused on developing targeted therapeutics in oncology, - announces the appointment of Scott Filosi as Chief Executive Officer (CEO), effective November 6, 2023. The company changes name to Evexta Bio, effective immediately. Dominique Bridon, former CEO, is appointed Chief Scientific Officer, and will remain as an executive and Board Member. Scott is an experienced executive leader with an outstanding track record in the pharmaceutical and biotechnology sector and as CEO. Scott brings more than 30 years of experience where he has put on the market more than 20 innovative medicines. Scott served as CEO of Luzsana Bio and Mirror Bio where he helped to advance key clinical programs, raise capital and advance strategic imperatives. Prior to his CEO roles, Scott was successively global Senior Vice President Market Access and Pricing and Chief Commercial Officer US for Merck KGaA successfully launching multiple oncology assets and indications. He brings diverse experience in sales, marketing, market access, pricing, operations and business development with organizations including UCB, J&J and Boehringer-Ingelheim. The Annual General Meeting also approved the change of company name to Evexta Bio. designed to better represent the company’s ability to advance rupitasertib through Phase 2/3 development, and to collaborate with partners for further development and commercialization. Along with the new name, the Company has adopted a new logo and is refreshing its corporate website to reflect the company’s strategy moving forward. Visit to learn more. Alain Chevallier, Chairman of the Board of Evexta Bio, commented:“The Board of Directors warmly welcomes Scott as the new CEO of Evexta Bio. Given his extensive international management experience in bringing successfully oncology drugs on the market, Scott is uniquely qualified to lead Evexta Bio's strategic development. He brings a unique set of skills, perspectives, and network to lead Evexta Bio into this new stage. I warmly thank Dominique for leading, during his tenure as CEO the shift of the company from a preclinical start-up to a late clinical stage biotech. I am pleased that he will continue to bring its tremendous scientific expertise to Evexta Bio as Chief Scientific Officer.” Scott Filosi, new CEO and Board Member of Evexta Bio,added: "I am thrilled to join Evexta Bio and its impressive team in a leadership position to advance its development strategy, and in particular, its clinical programs, both alone and in partnerships. I would like to thank Dominique for his dedication and look forward to building together on his achievements.” Dominique Bridon, PhD, CSO of Evexta Bio, said:“I am delighted to have Scott as the new CEO of Evexta Bio. With his impressive track record in the pharmaceutical and biotech industries, I believe Scott is the right person to lead the company through this important phase of development and partnering. I look forward to continuing to provide my scientific support to Evexta Bio.” ***** About Evexta Bio ( ) Evexta Bio, formerly Diaccurate, is a biopharmaceutical company exploring the new frontiers of oncology in search of daring novel therapeutic approaches with the potential to save lives. Now in the clinic, the French biotech is currently developing two proprietary therapeutic assets with novel mechanisms of action across several indications: Rupitasertib, formerly DIACC3010, an optimized S6K inhibitor with efficient AKT1/AKT3 control of feed-back loop. The oral anti-tumor agent is expected to enter phase 2/3 clinical trial in refractory ER+ HER2- metastatic breast cancer. EVX020, formerly DIACC2020, an antibody-drug conjugate program using a sole-in-class KIF20A kinesin inhibitor as payload in hematological and solid tumors. Founded by Truffle Capital, Evexta Bio has forged alliances with leaders in academia and industry, including CNRS, Paoli-Calmettes Institute (Marseille, France) and Merck KGaA (Darmstadt, Germany). The company is supported by seasoned management team, board of directors and medical advisory board. Contacts ATCG PARTNERS Marie Puvieux +33 (0)9 52 78 85 08 presse@atcg-partners.com Attachment PR in English

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RPS6KB1

Ribosomal protein S6 kinase beta-1

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