Truqap (capivasertib)
Research Synopsis
- Truqap (capivasertib) is being researched primarily for its effectiveness in treating advanced breast cancer when used in combination with fulvestrant.
- A significant study, termed the FAKTION trial, tested capivasertib against a placebo and demonstrated its potential to improve progression-free survival in women with metastatic, oestrogen receptor-positive breast cancer.
- The trial involved 140 participants and highlighted the importance of monitoring treatment effects over time, showcasing capivasertib's viability as a targeted therapy.
- In addition to breast cancer, capivasertib has shown promise in genetically profiling tumors, as seen in the VIKTORY trial for advanced stomach cancer, showcasing the trend toward personalized medicine.
- Capivasertib operates by inhibiting the AKT pathway, which is often activated in cancer cells, especially those with specific mutations (like PI3KCA or PTEN) that influence treatment efficacy.
- Research has indicated that capivasertib, when used alone or in combination with other treatment modalities, can lead to significant tumor growth inhibition, particularly in therapy-resistant cancer types.
- Preliminary results also suggest that capivasertib may enhance the effectiveness of standard treatments (like Taxotere) in certain gastric cancer models, potentially providing clinicians with more therapeutic options.
- Studies have focused on finding optimal combo therapies, such as pairing capivasertib with endocrine therapies in resistant breast cancer models, indicating a multifaceted approach to treatment.
- Overall, current developments position Truqap (capivasertib) as a crucial component of modern oncology, emphasizing the need for further clinical trials to solidify its therapeutic role and efficacy.
- Future research directions indicate a potential shift towards integrated treatments that leverage genetic profiling alongside targeted inhibitors to maximize patient outcomes in various cancer types.
Truqap (capivasertib)
Fulvestrant plus capivasertib versus placebo after relapse or progression on an aromatase inhibitor in metastatic, oestrogen receptor-positive breast cancer (FAKTION): a multicentre, randomised, controlled, phase 2 trial.
London, UK
2 hours ago
1 Received
- Capivasertib is a medicine being tested to see if it helps women with advanced breast cancer live longer without their disease getting worse when combined with another medicine called fulvestrant.
- Scientists conducted a trial where they gave one group of women capivasertib and another group a fake pill (placebo), while both groups received fulvestrant.
- The trial was carefully organized and included 140 women who qualified to participate, with results being tracked over time to see how effective the treatment was.
$100 - $150
Hourly Rate
Tumor Genomic Profiling Guides Patients with Metastatic Gastric Cancer to Targeted Treatment: The VIKTORY Umbrella Trial.
London, UK
2 hours ago
1 Received
- The VIKTORY trial looked at patients with advanced stomach cancer to find out how their tumors could guide treatment, using different markers to classify them into specific groups.
- A total of 772 patients took part, and they did genetic tests on most of them to find out which drugs might work best.
- The results were promising, showing that patients who got treatments matched to their tumor markers did better than those who just got standard chemotherapy.
$100 - $150
Hourly Rate
A conserved role for AKT in the replication of emerging flaviviruses in vertebrates and vectors.
London, UK
2 hours ago
1 Received
- One third of new diseases that spread are caused by insects like mosquitoes, and there are no approved medicines for these diseases.
- Zika and Usutu viruses, which are transmitted by mosquitoes, are studied to understand how they grow inside cells, focusing on a system called the PI3K/AKT/mTOR pathway.
- Researchers tested two medicines that block a part of this pathway and found that one worked better in human cells and the other worked better in mosquito cells, showing that the virus can affect different types of cells in different ways.
$100 - $150
Hourly Rate
Preclinical pharmacology of AZD5363, an inhibitor of AKT: pharmacodynamics, antitumor activity, and correlation of monotherapy activity with genetic background.
London, UK
2 hours ago
1 Received
- AKT is a crucial component in cancer signaling networks, and AZD5363 is a new compound that effectively inhibits all AKT isoforms at low concentrations.
- AZD5363 has been shown to reduce tumor cell growth in a variety of cancer types, particularly in breast cancer, and its effectiveness is influenced by specific genetic mutations (like PIK3CA and PTEN).
- Chronic oral administration of AZD5363 in mice demonstrated dose-dependent tumor growth inhibition and increased effectiveness when combined with other cancer treatments, highlighting its potential for clinical use and personalized medicine strategies.
$100 - $150
Hourly Rate
Blocked autophagy using lysosomotropic agents sensitizes resistant prostate tumor cells to the novel Akt inhibitor AZD5363.
London, UK
2 hours ago
1 Received
- Prostate cancer often develops due to the loss of PTEN, a key tumor suppressor that helps regulate the PI3K-Akt pathway, leading to therapy resistance, making this pathway a key target for cancer treatment.
- In this study, researchers tested the Akt inhibitor AZD5363 on prostate cancer cells, finding that while it effectively impacted downstream signaling, it didn't significantly induce cell death without help from other treatments.
- Combining AZD5363 with chloroquine (an autophagy inhibitor) led to a notable reduction in tumor volume in mouse models, suggesting that this combination could improve treatment efficacy in prostate cancer.
$100 - $150
Hourly Rate
Discovery of 4-amino-N-[(1S)-1-(4-chlorophenyl)-3-hydroxypropyl]-1-(7H-pyrrolo[2,3-d]pyrimidin-4-yl)piperidine-4-carboxamide (AZD5363), an orally bioavailable, potent inhibitor of Akt kinases.
London, UK
2 hours ago
1 Received
- A comprehensive study on variations of a pyrrolopyrimidine inhibitor targeting ATP led to the identification of AZD5363 as a promising drug candidate.
- AZD5363 exhibited enhanced effectiveness, lower affinity for the hERG channel, and greater selectivity towards AGC kinase ROCK compared to similar compounds.
- In preclinical tests, AZD5363 demonstrated favorable drug metabolism and pharmacokinetics, effectively reducing Akt phosphorylation and inhibiting tumor growth in breast cancer models after oral administration.
$100 - $150
Hourly Rate
Dual inhibition of autophagy and the AKT pathway in prostate cancer.
London, UK
2 hours ago
1 Received
- Genetic inactivation of PTEN is frequently observed in metastatic prostate cancer, activating the PI3K-AKT pathway, which is linked to poor patient outcomes.
- Despite attempts, existing therapies targeting the PI3K-AKT pathway have largely failed in trials, highlighting the need for new strategies.
- The study shows that the AKT inhibitor AZD5363 can induce cell growth arrest and enhance cell death when paired with chloroquine, offering a promising combination therapy for treating resistant prostate cancer.
$100 - $150
Hourly Rate
2-Deoxy-2-[18F]fluoro-D-glucose positron emission tomography demonstrates target inhibition with the potential to predict anti-tumour activity following treatment with the AKT inhibitor AZD5363.
London, UK
2 hours ago
1 Received
- - The study investigates the use of 18F-FDG PET scans as a biomarker to evaluate the effectiveness of AZD5363, an AKT inhibitor in cancer treatment, particularly focusing on its impact on glucose metabolism in tumor cells.
- - Results show that a single dose of AZD5363 led to a significant 39% reduction in 18F-FDG uptake in tumor xenografts after only 4 hours, indicating its effectiveness in inhibiting the AKT pathway, with multiple doses further diminishing tumor volume and glucose uptake.
- - The research concludes that 18F-FDG PET is a valuable pharmacodynamic biomarker for assessing the inhibition of the AKT pathway, which could guide treatment decisions and improve outcomes by identifying
$100 - $150
Hourly Rate
The AKT inhibitor AZD5363 is selectively active in PI3KCA mutant gastric cancer, and sensitizes a patient-derived gastric cancer xenograft model with PTEN loss to Taxotere.
London, UK
2 hours ago
1 Received
- The activation of the PI3K/AKT pathway is common in cancer, often due to mutations in genes like PI3KCA and PTEN, leading to the development of an AKT inhibitor called AZD5363 that showed effectiveness against gastric cancer (GC) cells with these mutations.
- Research on 20 GC cell lines and tumor samples from Chinese patients revealed that those with PI3KCA mutations responded better to AZD5363 and highlighted the prevalence of these mutations and PTEN loss in the patient cohort.
- The study concluded that PI3KCA mutation is key for predicting response to AKT inhibitors, and combining AZD5363 with Taxotere could enhance treatment efficacy in patients with PTEN loss,
$100 - $150
Hourly Rate
Synergistic targeting of PI3K/AKT pathway and androgen receptor axis significantly delays castration-resistant prostate cancer progression in vivo.
London, UK
2 hours ago
1 Received
- The study explores how combining an AKT inhibitor (AZD5363) with an antiandrogen (bicalutamide) can enhance treatment effectiveness for castration-resistant prostate cancer (CRPC), compared to using either drug alone.
- It was found that while AZD5363 initially inhibits tumor growth and PSA levels, resistance develops after about 30 days due to increased androgen receptor activity.
- The combination of the two drugs leads to better inhibition of cancer cell growth and prolonged treatment benefits, suggesting a promising strategy for managing CRPC.
$100 - $150
Hourly Rate
Clusterin facilitates stress-induced lipidation of LC3 and autophagosome biogenesis to enhance cancer cell survival.
London, UK
2 hours ago
1 Received
- The research identifies how the molecular chaperone clusterin (CLU) interacts with autophagy processes to help cancer cells survive stress from treatment, promoting resistance to anticancer therapies.
- CLU aids in the formation and stability of autophagosomes, crucial for cell survival under treatment stress, and its absence leads to decreased autophagy and increased cell death in prostate cancer.
- Combining CLU inhibition with cancer treatments disrupts this survival mechanism, enhances cancer cell death, and potentially slows down cancer progression, suggesting a new approach for therapy.
$100 - $150
Hourly Rate
Autocrine IGF-I/insulin receptor axis compensates for inhibition of AKT in ER-positive breast cancer cells with resistance to estrogen deprivation.
London, UK
2 hours ago
1 Received
- - Estrogen receptor α-positive (ER+) breast cancers can develop resistance to antiestrogen therapies, leading to a heightened reliance on the PI3K/AKT signaling pathway, which is crucial for their survival post-hormone deprivation.
- - Researchers tested the AKT inhibitor AZD5363 on resistant ER+ breast cancer cell lines and found it effectively reduced cell growth and phosphorylation of specific proteins, indicating that it could block cancer progression.
- - Combining AZD5363 with another treatment, fulvestrant, enhanced the anti-cancer effects more than using either drug solo, although it also triggered compensatory activation of insulin-related signaling pathways in the resistant cells.
$100 - $150
Hourly Rate
Stimulus-dependent differences in signalling regulate epithelial-mesenchymal plasticity and change the effects of drugs in breast cancer cell lines.
London, UK
2 hours ago
1 Received
- The process of epithelial-mesenchymal transition (EMT) has been altered by carcinoma cells, leading to a state called epithelial-mesenchymal plasticity (EMP), which is linked to increased metastatic risk and poor breast cancer prognosis.
- The study examined EMP in breast cancer cell lines, using EGF stimulation and hypoxic conditions to transition cells to a mesenchymal phenotype and analyzed gene expression changes through RNA sequencing.
- Results showed that EGF and hypoxia induce similar mesenchymal states in breast cancer cells, but revealed differing cellular signaling pathways and responses to treatment with chemical inhibitors.
$100 - $150
Hourly Rate
High Efficacy of Combination Therapy Using PI3K/AKT Inhibitors with Androgen Deprivation in Prostate Cancer Preclinical Models.
London, UK
2 hours ago
1 Received
- The PI3K/AKT pathway is often activated during prostate cancer (PCa) progression, particularly due to PTEN gene mutations, making it a major target for treatment alongside the androgen receptor pathway.
- Researchers tested the effectiveness of AZD5363 and AZD8186, two PI3K/AKT inhibitors, on 12 human PCa cell lines and evaluated their combination with androgen deprivation in vivo using mouse models.
- The results showed significant growth inhibition in both in vitro and in vivo models, especially for PTEN-negative tumors, with the combination treatment leading to lasting tumor regression and upregulation of certain androgen receptor target genes.
$100 - $150
Hourly Rate
Combination AZD5363 with Enzalutamide Significantly Delays Enzalutamide-resistant Prostate Cancer in Preclinical Models.
London, UK
2 hours ago
1 Received
- - The study investigates the effects of AZD5363, an Akt inhibitor, alone and with enzalutamide (ENZ) in castrate-resistant prostate cancer (CRPC), finding that AZD5363 effectively induces cell death and inhibits tumor growth in ENZ-resistant cancer models.
- - The combination of AZD5363 and ENZ demonstrated a greater impact on reducing cell proliferation, inducing cell-cycle arrest, and causing tumor regression in models compared to using either drug alone, with no signs of tumor recurrence noted.
- - Overall, the research suggests that combining AZD5363 and ENZ can significantly delay the onset of resistance in prostate cancer treatment, indicating potential for improved clinical outcomes if used earlier in treatment.
$100 - $150
Hourly Rate
Validation of a predictive modeling approach to demonstrate the relative efficacy of three different schedules of the AKT inhibitor AZD5363.
London, UK
2 hours ago
1 Received
- This study explores the effectiveness of intermittent dosing of the AKT inhibitor AZD5363 compared to continuous dosing in order to improve cancer treatment outcomes.
- A mathematical model was developed to analyze the pharmacokinetics and anti-tumor effects of AZD5363, showing that both continuous and intermittent dosing inhibited tumor growth, with higher intermittent doses leading to increased cancer cell death.
- The findings suggest that using intermittent dosing can achieve similar anti-tumor effects as continuous dosing at higher doses, allowing for better tolerability and flexibility in treatment schedules, especially in combination with other therapies like chemotherapy.
$100 - $150
Hourly Rate
Combining AZD8931, a novel EGFR/HER2/HER3 signalling inhibitor, with AZD5363 limits AKT inhibitor induced feedback and enhances antitumour efficacy in HER2-amplified breast cancer models.
London, UK
2 hours ago
1 Received
- The PI3K/AKT/mTOR signaling network is often disrupted in breast cancer, contributing to resistance against anti-HER2 treatments and hindering the effectiveness of PI3K inhibitors due to feedback loops that reactivate HER2/HER3.
- A study tested the combination of AZD5363 (an AKT inhibitor) and AZD8931 (an EGFR/HER2/HER3 inhibitor) on breast cancer cells, finding that this combination significantly increased tumor cell death and growth inhibition, especially in cells with HER2 amplification.
- In a resistant xenograft model, the dual treatment showed greater efficacy than either drug alone, suggesting that targeting both AKT and HER2-related pathways could be a promising strategy
$100 - $150
Hourly Rate
Complex impacts of PI3K/AKT inhibitors to androgen receptor gene expression in prostate cancer cells.
London, UK
2 hours ago
1 Received
- Androgen deprivation therapy (ADT) is the standard treatment for metastatic prostate cancer, but many tumors eventually become resistant, partly due to ongoing activity of the androgen receptor (AR) and adaptation of the PI3K/AKT pathway.
- Co-targeting AR and the PI3K/AKT signaling pathway has emerged as a potential strategy for treating these castration-resistant cases, and clinical trials are currently exploring the effectiveness of PI3K/AKT inhibitors for this purpose.
- The study found that these inhibitors influence AR expression in various prostate cancer cell lines by affecting gene transcription and RNA splicing, highlighting the need to consider these effects when using inhibitors in patients undergoing ADT.
$100 - $150
Hourly Rate
AKT Antagonist AZD5363 Influences Estrogen Receptor Function in Endocrine-Resistant Breast Cancer and Synergizes with Fulvestrant (ICI182780) In Vivo.
London, UK
2 hours ago
1 Received
- PI3K/AKT/mTOR signaling is crucial in breast cancer, particularly in the context of estrogen receptor (ER) signaling and acquired endocrine resistance, making treatment challenging.
- Targeting mTOR along with endocrine therapy has clinical benefits, but a negative feedback mechanism complicates outcomes, suggesting that directly inhibiting AKT may enhance treatment efficacy.
- AZD5363, a new AKT inhibitor, demonstrates promising results in resensitizing tamoxifen-resistant breast cancer cells and shows potential in combination with fulvestrant, indicating its value for future clinical trials.
$100 - $150
Hourly Rate
Co-treatment of Salinomycin Sensitizes AZD5363-treated Cancer Cells Through Increased Apoptosis.
London, UK
2 hours ago
1 Received
- * The study found that combining AZD5363 with low levels of salinomycin effectively reduces the growth of breast cancer cells by promoting apoptosis and S-phase arrest.
- * These findings suggest that salinomycin could enhance the effectiveness of AZD5363, potentially leading to better cancer treatment options in the future.
$100 - $150
Hourly Rate