What side effects are associated with this type of intervention?

Common treatments for solid tumors, particularly those that interfere with DNA repair mechanisms such as DNA-damage response agents, often have a range of side effects. These can include hematologic toxicities like anemia, thrombocytopenia, and neutropenia, which are frequently severe (grade 3 or 4). Non-hematologic side effects may include nausea, vomiting, fatigue, diarrhea, and neuropathy. Additionally, patients may experience increased susceptibility to infections, cardiovascular issues, and secondary cancers. The severity and occurrence of these side effects can vary based on the specific treatment regimen and patient factors.

What prior FDA approvals exist?

The FDA has approved several DNA-damage response agents for the treatment of solid tumors. Notable among these are PARP inhibitors such as olaparib, rucaparib, and niraparib, which are used in ovarian, breast, and prostate cancers. These drugs inhibit the PARP enzyme, essential for repairing single-strand DNA breaks, leading to cancer cell death. These approvals highlight the therapeutic potential of targeting DNA repair mechanisms in cancer treatment.

What other types of research exist?

Promising novel alternatives to DNA-damage Response Agents for solid tumor patients include: 1) ONC201, an investigational oral compound targeting mitochondrial metabolism and stress response pathways, particularly effective in H3 K27M-mutant gliomas. 2) Chimeric Antigen Receptor (CAR) T-cell therapy targeting GD2, a surface marker on H3 K27M-mutant glioma cells. 3) DNX-2401, an oncolytic adenovirus administered locally to target tumor cells. These therapies are under active investigation and have shown potential in early clinical trials.

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DNA-damage Response Agent

Ceralasertib for Advanced Cancer

Phase 2

Waitlist Available

Research Sponsored by AstraZeneca

Eligibility Criteria Checklist

Specific guidelines that determine who can or cannot participate in a clinical trial

Must have

Documented prostate cancer progression at study entry while on androgen deprivation or after bilateral orchiectomy as assessed by the investigator.

Participants must have a histologically confirmed diagnosis of AST (excluding NSCLC) or mCRPC tumour.

Must not have

Acute myocardial infarction.

Exposure to a small molecule investigational product within 14 days or 5 half-lives.

Timeline

Screening 3 weeks

Treatment Varies

Follow Up 2 years 4 months

Awards & highlights

No Placebo-Only Group

Summary

This trial tests a medication in patients with advanced solid tumors or metastatic prostate cancer. It targets those with specific molecular changes in their tumors. The drug works by stopping cancer cells from repairing their DNA, making it harder for them to survive.

Who is the study for?

This trial is for adults with advanced solid tumors containing specific ATM mutations, who have progressed on certain treatments like hormonal agents for prostate cancer. They must have normal organ and bone marrow function, no curative treatment options available, and can't join if they've had recent heart issues, uncontrolled medical conditions or infections.

What is being tested?

The study tests the effectiveness of Ceralasertib in treating advanced cancers with ATM mutations. It looks at how safe it is and what side effects occur when used alone or combined with other drugs. Participants are selected based on their genetic profile related to these mutations.

What are the potential side effects?

While not explicitly listed in the provided information, DNA-damage response agents like Ceralasertib may cause fatigue, nausea, blood count changes leading to increased infection risk or bleeding problems, liver function abnormalities and potential allergic reactions.

Eligibility Criteria

Inclusion Criteria

You may be eligible if you check “Yes” for the criteria below

Select...

You have already tried and your cancer got worse while taking at least one newer type of hormone treatment for prostate cancer, such as abiraterone acetate, apalutamide, or enzalutamide.

Exclusion Criteria

You may be eligible for the trial if you check “No” for criteria below:

Select...

You have brain metastases that are causing symptoms or are not well controlled.

Select...

You have previously received a medication called a telangiectasia and rad3 related protein inhibitor.

Timeline

Screening ~ 3 weeks3 visits

Treatment ~ Varies

Follow Up ~ 2 years 4 months

Screening ~ 3 weeks

Treatment ~ Varies

Follow Up ~2 years 4 months

This trial's timeline: 3 weeks for screening, Varies for treatment, and 2 years 4 months for reporting.

Treatment Details

Study Objectives

Study objectives can provide a clearer picture of what you can expect from a treatment.

Primary study objectives

Cohort A (aST): Objective Response Rate (ORR).

Cohort B (mCRPC): Composite Response Rate.

Secondary study objectives

Cohort A (aST) and B (mCRPC): Number of Participants With Serious and Non-serious Adverse Events

Cohort A (aST): Duration of Radiological Response (DoR)

Cohort A (aST): Percentage Change in Tumor Size

+2 more

Awards & Highlights

No Placebo-Only Group

All patients enrolled in this study will receive some form of active treatment.

Trial Design

2Treatment groups

Experimental Treatment

Group I: Cohort BExperimental Treatment1 Intervention

Eligible participants (ATM altered mCRPC), will receive oral dose of Ceralasertib as monotherapy.

Group II: Cohort AExperimental Treatment1 Intervention

Eligible participants (ATM altered AST), will receive oral dose of Ceralasertib as monotherapy.

Treatment

First Studied

Drug Approval Stage

How many patients have taken this drug

Ceralasertib

2017

Completed Phase 1

~40

0 / 12Eligibility criteria met

Research Highlights

Information in this section is not a recommendation. We encourage patients to speak with their healthcare team when evaluating any treatment decision.

Mechanism Of Action

Side Effect Profile

Prior Approvals

Other Research

DNA-damage response agents, commonly used in the treatment of solid tumors, work by interfering with the DNA repair mechanisms in cancer cells. These agents inhibit the pathways that cancer cells use to repair their DNA, causing an accumulation of DNA damage that ultimately leads to cell death. This mechanism is particularly important for solid tumor patients because their tumors often have high rates of genetic mutations and depend heavily on DNA repair for survival. By targeting these repair pathways, these treatments can selectively kill cancer cells, offering a potentially more effective and less toxic therapeutic option.