On April 17, 2018 Arcus Biosciences, Inc. (NYSE:RCUS), a clinical-stage biopharmaceutical company focused on creating innovative cancer immunotherapies, reported that it will present data today from its Phase 1 trial for AB928, its dual adenosine receptor antagonist, in healthy volunteers in a poster presentation titled "Clinical Pharmacokinetic-Pharmacodynamic Relationship for AB928, a Dual Antagonist of the A2aR and A2bR Adenosine Receptors," at the 2018 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in Chicago, Illinois (Press release, Arcus Biosciences, APR 17, 2018, View Source [SID1234525418]).

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"We are extremely encouraged by the results from our ongoing Phase 1 trial of AB928. The compound has been shown to be safe and well tolerated at all doses evaluated and achieves near complete inhibition of A2aR adenosine receptor activation in blood samples from healthy volunteers," said Terry Rosen, Ph.D., Chief Executive Officer at Arcus. "Importantly, we achieved this level of inhibition under conditions that we believe are representative of the large concentrations of adenosine found in the tumor microenvironment. These results have informed the selection of the starting dose for our clinical trials of AB928 in combination with other anti-cancer agents, and we look forward to starting these trials shortly."

Design of the Phase 1 Trial for AB928 in Healthy Volunteers
The Phase 1 double-blinded, placebo-controlled trial has enrolled 85 healthy volunteers. The trial includes a single-ascending-dose (SAD) portion as well as a multiple-ascending-dose (MAD) portion. In the SAD portion, single doses of 10, 25, 75 and 150 mg and a twice-daily dose of 100 mg have been evaluated. In the MAD portion, doses of 10, 25, 75 and 150 mg QD and 200 mg QD (with food) have been administered to subjects for four consecutive days. In each dosing cohort, 6 subjects received AB928 and 2 subjects received placebo, and dosing in the trial has been completed. Investigators remain blinded regarding subject assignment to the AB928 or placebo arms.
The objective of this trial is to assess the safety, tolerability, pharmacokinetics and pharmacodynamic profile of AB928 and to inform our selection of the starting dose of AB928 for our combination trials in cancer patients.

Summary of the Results Presented
All doses have been safe and well tolerated, and no safety events prevented escalation to higher doses. To assess the pharmacodynamic effects of AB928, blood samples were taken from subjects at different time points following the administration of AB928 or placebo. As of the cut-off date (COD) of March 30, 2018 for the poster presentation, samples from all dosing cohorts, with the exception of the 200 mg QD (with food) MAD cohort, have been evaluated to assess the pharmacodynamic effects of AB928. These samples were treated with NECA (a synthetic analogue of adenosine), which activates A2aR receptors on T cells. The ability of AB928 to block A2aR receptors on T cells was quantified by measuring the levels of pCREB, which is a marker for activation of the A2aR receptor.
When blood samples from the 150 mg MAD cohort were incubated with 5 µM NECA, AB928 achieved complete inhibition of pCREB activation at two hours post-dosing and approximately 90% mean inhibition of pCREB activation at 24 hours post-dosing on day 4. As experiments conducted in vitro by Arcus have demonstrated that NECA is at least 20 times more potent than adenosine at inducing pCREB activation in blood T cells, stimulation with 5 µM NECA should be comparable to stimulation with adenosine concentrations in excess of 100 µM.
The pharmacokinetic profile of AB928 supports once-daily dosing, with a plasma half-life that exceeds 20 hours.
Complete results from this trial, including pharmacodynamic data for the 200 mg BID (with food) dosing cohort, will be released following the unblinding of data in mid-2018.

AB928 Clinical Development Plans
The results from this healthy volunteer trial demonstrate that a safe and well tolerated dose of AB928 can provide near complete inhibition of A2aR receptor activation. Based on these results, Arcus is preparing to initiate clinical trials to evaluate AB928 in combination with three different chemotherapy regimens and in combination with AB122, its PD-1 antibody, in cancer patients. Regulatory submissions to start these trials are underway.
These trials will include a dose-escalation portion to identify the recommended dose of AB928 for each combination regimen. Based on the safety profile of AB928, the initial dose of AB928 for the dose-escalation portion should achieve close to complete inhibition of A2aR receptor activation. Once the recommended dose has been selected, AB928 will be evaluated in 11 expansion cohorts. Each expansion cohort will evaluate the AB928 + chemotherapy combination and/or the AB928 + AB122 combination in one of the following tumor types: non-small cell lung cancer, renal cell carcinoma, gastroesophageal cancer, colorectal cancer, ovarian cancer and triple negative breast cancer. In both the dose escalation portion and expansion cohorts, Arcus will conduct significant biomarker analysis, which will inform patient selection in future trials. Arcus plans to report data from the dose-escalation portion of these trials in the first half of 2019

On April 17, 2018 Genmab A/S (Nasdaq Copenhagen: GEN) reported that worldwide net sales of DARZALEX (daratumumab) as reported by Johnson & Johnson were USD 432 million in the first quarter of 2018 (Press release, Genmab, APR 17, 2018, View Source [SID1234525439]). Net sales were USD 264 million in the U.S. and USD 168 million in the rest of the world. Genmab will receive royalties on the worldwide net sales of DARZALEX under the exclusive worldwide license to Janssen Biotech, Inc. to develop, manufacture and commercialize DARZALEX.

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About DARZALEX (daratumumab)
DARZALEX (daratumumab) injection for intravenous infusion is indicated in the United States in combination with lenalidomide and dexamethasone, or bortezomib and dexamethasone, for the treatment of patients with multiple myeloma who have received at least one prior therapy; in combination with pomalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received at least two prior therapies, including lenalidomide and a proteasome inhibitor (PI); and as a monotherapy for the treatment of patients with multiple myeloma who have received at least three prior lines of therapy, including a PI and an immunomodulatory agent, or who are double-refractory to a PI and an immunomodulatory agent.1 DARZALEX is the first monoclonal antibody (mAb) to receive U.S. Food and Drug Administration (FDA) approval to treat multiple myeloma. DARZALEX is indicated in Europe for use in combination with lenalidomide and dexamethasone, or bortezomib and dexamethasone, for the treatment of adult patients with multiple myeloma who have received at least one prior therapy and as monotherapy for the treatment of adult patients with relapsed and refractory multiple myeloma, whose prior therapy included a PI and an immunomodulatory agent and who have demonstrated disease progression on the last therapy. In Japan, DARZALEX is approved in combination with lenalidomide and dexamethasone, or bortezomib and dexamethasone, for treatment of adults with relapsed or refractory multiple myeloma. DARZALEX is the first human CD38 monoclonal antibody to reach the market. For more information, visit www.DARZALEX.com.
Daratumumab is a human IgG1k monoclonal antibody (mAb) that binds with high affinity to the CD38 molecule, which is highly expressed on the surface of multiple myeloma cells. Daratumumab triggers a person’s own immune system to attack the cancer cells, resulting in rapid tumor cell death through multiple immune-mediated mechanisms of action and through immunomodulatory effects, in addition to direct tumor cell death, via apoptosis (programmed cell death).1,2,3,4,5

Daratumumab is being developed by Janssen Biotech, Inc. under an exclusive worldwide license to develop, manufacture and commercialize daratumumab from Genmab. A comprehensive clinical development program for daratumumab is ongoing, including multiple Phase III studies in smoldering, relapsed and frontline multiple myeloma settings and in amyloidosis. Additional studies are ongoing or planned to assess the potential of daratumumab in other malignant and pre-malignant diseases, such as NKT-cell lymphoma, myelodysplastic syndromes, B and T-ALL and selected solid tumors. Daratumumab has received two Breakthrough Therapy Designations from the U.S. FDA, for multiple myeloma, as both a monotherapy and in combination with other therapies.. Net sales were USD 264 million in the U.S. and USD 168 million in the rest of the world. Genmab will receive royalties on the worldwide net sales of DARZALEX under the exclusive worldwide license to Janssen Biotech, Inc. to develop, manufacture and commercialize DARZALEX.

About DARZALEX (daratumumab)
DARZALEX (daratumumab) injection for intravenous infusion is indicated in the United States in combination with lenalidomide and dexamethasone, or bortezomib and dexamethasone, for the treatment of patients with multiple myeloma who have received at least one prior therapy; in combination with pomalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received at least two prior therapies, including lenalidomide and a proteasome inhibitor (PI); and as a monotherapy for the treatment of patients with multiple myeloma who have received at least three prior lines of therapy, including a PI and an immunomodulatory agent, or who are double-refractory to a PI and an immunomodulatory agent.1 DARZALEX is the first monoclonal antibody (mAb) to receive U.S. Food and Drug Administration (FDA) approval to treat multiple myeloma. DARZALEX is indicated in Europe for use in combination with lenalidomide and dexamethasone, or bortezomib and dexamethasone, for the treatment of adult patients with multiple myeloma who have received at least one prior therapy and as monotherapy for the treatment of adult patients with relapsed and refractory multiple myeloma, whose prior therapy included a PI and an immunomodulatory agent and who have demonstrated disease progression on the last therapy. In Japan, DARZALEX is approved in combination with lenalidomide and dexamethasone, or bortezomib and dexamethasone, for treatment of adults with relapsed or refractory multiple myeloma. DARZALEX is the first human CD38 monoclonal antibody to reach the market. For more information, visit www.DARZALEX.com.
Daratumumab is a human IgG1k monoclonal antibody (mAb) that binds with high affinity to the CD38 molecule, which is highly expressed on the surface of multiple myeloma cells. Daratumumab triggers a person’s own immune system to attack the cancer cells, resulting in rapid tumor cell death through multiple immune-mediated mechanisms of action and through immunomodulatory effects, in addition to direct tumor cell death, via apoptosis (programmed cell death).1,2,3,4,5

Daratumumab is being developed by Janssen Biotech, Inc. under an exclusive worldwide license to develop, manufacture and commercialize daratumumab from Genmab. A comprehensive clinical development program for daratumumab is ongoing, including multiple Phase III studies in smoldering, relapsed and frontline multiple myeloma settings and in amyloidosis. Additional studies are ongoing or planned to assess the potential of daratumumab in other malignant and pre-malignant diseases, such as NKT-cell lymphoma, myelodysplastic syndromes, B and T-ALL and selected solid tumors. Daratumumab has received two Breakthrough Therapy Designations from the U.S. FDA, for multiple myeloma, as both a monotherapy and in combination with other therapies.

On April 17, 2018 ArQule, Inc. (NASDAQ:ARQL) reported that it has entered into an exclusive license agreement with Basilea Pharmaceutica International Limited(Basilea, SIX: BSLN) to develop and commercialize derazantinib, a pan-FGFR (fibroblast growth factor receptor) inhibitor in the US, EU, Japan and rest of the world excluding the People’s Republic of China, Hong Kong, Macau and Taiwan, where Sinovant Sciences Ltd., a Roivant Sciences Ltd. subsidiary, has rights to develop and exclusively commercialize the drug (Press release, ArQule, APR 17, 2018, View Source [SID1234525419]).

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Under the terms of the agreement, ArQule will receive an upfront payment of $10 million and is eligible for up to $326 million in regulatory and commercial milestones. ArQule is also entitled to receive staggered single-digit to double-digit royalties on net sales upon commercialization. Basilea will be responsible for all costs and expenses of development, manufacture and commercialization in its territory. Under certain circumstances, ArQule may have the opportunity to promote derazantinib in the US directly.
ArQule is currently conducting a registrational trial for derazantinib in the United States, Canada and Europe as a potential treatment for intrahepatic cholangiocarcinoma (iCCA), a form of biliary tract cancer. As part of the exclusive license agreement, Basilea intends to continue this trial and the further development of derazantinib in iCCA and other tumor types with FGFR dysregulation.

Ronald Scott, Chief Executive Officer of Basilea, said: "We are very excited about this partnership with ArQule. Derazantinib is an ideal match for our existing clinical oncology portfolio. It is a targeted therapy building on a solid biomarker approach in an area where patients currently have limited treatment options. This transaction underscores our continued commitment to expand our R&D portfolio with novel compounds focused on overcoming the clinical problem of resistance in oncology and infectious diseases. Our clinical oncology portfolio now includes three drug candidates in different stages of development. We continue to focus on further broadening our R&D portfolio through internal and external innovation."

"Partnering with Basilea, a company with global drug development experience and expertise, will propel the advancement of derazantinib in ways we could not have achieved independently," said Paolo Pucci, Chief Executive Officer of ArQule. "Basilea will bring a wealth of skills to the expansion of the derazantinib development plan at a time when it will benefit most from these resources, allowing it to reach its full potential in iCCA and beyond."
ArQule will hold a conference call to discuss this agreement tomorrow, April 18, beginning at 9 a.m. EDT. Paolo Pucci, Chief Executive Officer of ArQule, will lead the call. As a result of entering into the exclusive license agreement, ArQule will be updating its financial guidance on the call.

The details of the call are as follows:
Wednesday, April 18, 2018 at 9:00 AM EDT
Audio connection numbers:
US: 1 877-868-1831
Outside US: 1 914-495-8595 PIN: 4089669
A replay of the call will be available two hours after the completion of the call and can be accessed in the "Investors and Media" section of our website, www.arqule.com, under "Events and Presentations." The ArQule investor conference call will be archived and can be accessed in the "Investors and Media" section of ArQule’s website, www.arqule.com, under "Events and Presentations."
About Derazantinib
Derazantinib is a potent, orally administered inhibitor of the fibroblast growth factor receptor (FGFR) family, a key driver of cell proliferation, differentiation, and migration. In a Phase 1/2 study in patients with iCCA harboring FGFR2 gene fusions, treatment with derazantinib resulted in an objective response rate of 21%, nearly 3 times higher than standard-of-care chemotherapy. ArQule is currently conducting a registrational study with derazantinib in patients with FGFR2 fusion-positive second-line iCCA. The open-label single-arm trial is recruiting in the United States, Canada and Europe with objective response rate as the primary endpoint. More information on that program is available here.
About Intrahepatic Cholangiocarcinoma
Cholangiocarcinoma (CCA) is the most common biliary malignancy and the second most common hepatic malignancy after hepatocellular carcinoma (HCC).1 Depending on the anatomic location, CCA is classified as intrahepatic (iCCA), perihilar (pCCA), and extrahepatic (eCCA). iCCA originates from the intrahepatic biliary ductal system and forms an intrahepatic mass. iCCA is an aggressive cancer, with a median 5-year survival rate of 15% for patients diagnosed with early-stage disease.2 In China, the incidence of cholangiocarcinoma is more than 7 cases per 100,000 people, and the majority of cases are intrahepatic.3

On April 17, 2018 H3 Biomedicine Inc., a clinical stage biopharmaceutical company specializing in the discovery and development of next-generation cancer medicines using its data science and precision chemistry product engine, reported novel findings from a comprehensive genomic analysis of 6,235 patients across 15 hematologic malignancies (Press release, H3 Biomedicine, APR 17, 2018, View Source [SID1234525440]). The results include the first-ever observance of recurrent RNA splicing factor mutations in non-Hodgkin’s lymphoma (NHL) and multiple myeloma (MM). While splicing factor mutations have been observed in other hematologic malignancies, including myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML) and chronic lymphocytic leukemia (CLL), the presence of these mutations in NHL and MM has not been reported previously.

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Presented today at the 2018 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in Chicago, these new findings demonstrate the continued emergence of splicing factor mutations as a hallmark of dozens of hematologic and solid tumor cancers, their potential role in tumor formation and growth, and, thus, the opportunity to advance a new class of therapies.
At the AACR (Free AACR Whitepaper) meeting, Dominic Reynolds, Ph.D., Vice President of Chemistry at H3 Biomedicine, also gave an oral presentation discussing the discovery of H3B-8800, the Company’s first-in-class potent, selective and orally bioavailable small molecule modulator of the SF3b complex currently in Phase I clinical trials in patients with AML, CMML and MDS with splicing factor mutations.
"We continue to uncover new insights into the prevalence of splicing factor mutations across a broad spectrum of hematologic and solid tumor cancers and are leveraging this knowledge for our existing development programs and to inform the discovery of new targets and drugs," said Peter Smith, Ph.D., chief scientific officer at H3 Biomedicine. "For example, our work presented at AACR (Free AACR Whitepaper) describes mutations that are addressed by our lead splicing modulator, H3B-8800, which we’re already evaluating in AML, MDS and CMML patients in an ongoing Phase 1 clinical study. These new findings of mutations in non-Hodgkin’s lymphoma and multiple myeloma could expand the addressable patient population for H3B-8800."

Dr. Smith continued, "Beyond our own development efforts, we hope the novel insights from this research will help advance the oncology community’s understanding of the pathogenesis of multiple myeloma and non-Hodgkin’s lymphoma and stimulate new drug discovery programs to help patients whose cancer cannot be effectively treated or cured with existing therapies."

The findings presented today were the result of an ongoing collaboration between H3 Biomedicine and Foundation Medicine Inc. (NASDAQ:FMI) to help advance the discovery and development of precision medicines in oncology. H3 Biomedicine scientists and scientists from Foundation Medicine jointly uncovered the mutations through computational biology based on the genomics data from FoundationOneHeme, Foundation Medicine’s comprehensive genomic profiling (CGP) assay for hematologic malignancies and sarcomas. H3 Biomedicine is now performing additional translational research to validate the findings.
"Comprehensive genomic profiling (CGP) is a critical tool to drive the discovery and development of precision medicines in both hematologic and solid tumor cancers," said Vincent Miller, M.D., chief medical officer at Foundation Medicine. "The inherent complexity of all cancers mandates the use of an unbiased comprehensive approach in genomic profiling to speed target identification and therapeutic options. These results obtained using FoundationOneHeme and our FoundationCore database further underscore that premise. We look forward to understanding how these findings may translate to potential new therapeutic strategies for patients."

About the Findings
H3 Biomedicine and Foundation Medicine scientists surveyed somatic mutations of several splicing factors (SF3B1, SRSF2, U2AF1, ZRSR2, DDX3X, ZMYM3, PCBP1 and U2AF2) in 6,235 patients across 15 hematological malignancies. While these mutations have been observed in MDS, AML, CMML and CLL, the frequency of these mutations in other hematological malignancies was unknown. In the analysis, 405 genes were analyzed by DNA sequencing using FoundationOneHeme,

The researchers, for the first time, identified splicing factor mutations in NHL (13.8%) and MM (9%), including hotspot somatic mutations of SF3B1, U2AF1 and SRSF2, and loss of function or missense mutations in DDX3X.
NHL-Specific Highlights
Among NHL patients, diffuse large B-cell lymphoma (DLBCL) demonstrated the highest frequency of splicing factor mutations, and these patients exhibited increased tumor mutation burden.
The RNA helicase DDX3X (an enzyme implicated in several types of cancer) was the most frequently mutated in NHL.
The majority of mutations were loss of function or missense mutations, suggesting a pathological relevance of DDX3X in lymphoid malignancies

.
MM-Specific Highlights
Among MM patients, SF3B1 and SRSF2 were the two most frequently mutated genes, and patients with these mutations also exhibited increased tumor mutation burden.
Although the most common SF3B1 mutation in hematopoietic malignancies is p.K700E, the findings revealed the most frequent SF3B1 mutation in MM is p.K666.

Findings Across All 15 Hematologic Malignancies
Consistent with prior reports, the hematopoietic malignancies that demonstrated the most frequent splicing factor mutations were CMML, MDS, AML and CLL.

In addition to mutations found across the different hematopoietic malignancies in the genes SRSF2, SF3B1, U2AF1 and ZRSR2, the researchers found DDX3X to be the fifth most frequently mutated gene, followed by ZMYM3, PCBP1 and U2AF2, indicating the importance of splicing dysregulation in hematological malignancies.
For additional details, please clink here to review the abstract.
The novel discovery of splicing factor mutations in NHL and MM underscores the potential of H3’s product engine to identify previously unknown cancer drivers for the discovery and development of next-generation targeted cancer therapies. Splicing modulation is one of several research focus areas for H3.

About RNA Splicing Factor Mutations
RNA splicing is the biological process by which pre-cursor messenger RNA (pre-mRNA) is edited into a mature messenger RNA (mRNA) and, ultimately, translated into a protein. Splicing factors carry out the editing process. They are responsible for removing introns, which are a part of a pre-mRNA molecule that do not code for proteins. When RNA splicing factors are mutated, normal RNA splicing becomes aberrant, leading to gene and protein expression changes that likely play a role in tumorigenesis
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About H3B-8800 – H3 Biomedicine’s First-in-Class Splicing Modulator
H3 Biomedicine is advancing novel cancer therapies that target core splicing factor mutations. A Phase 1 study is underway in patients with hematologic malignancies for H3B-8800, H3 Biomedicine’s first spliceosome pathway-targeting cancer therapeutic. H3B-8800 is a potent, selective and orally bioavailable small molecule modulator of wild-type and mutant SF3b complex, a splicing factor gene. The Phase 1 study is evaluating the safety and preliminary efficacy of H3B-8800 in patients with myelodysplastic syndromes, acute myeloid leukemia, and chronic myelomonocytic leukemia who carry mutations in splicing factor genes. In February 2018, H3 Biomedicine published preclinical data in Nature Medicine demonstrating that H3B-8800 modulates RNA splicing and shows preferential antitumor activity in a range of spliceosome-mutant cancer models.

On April 17, 2018 Tocagen Inc. (Nasdaq: TOCA), a clinical-stage, cancer-selective gene therapy company, reported updated durable response data from the Phase 1 study involving patients with high-grade glioma who received Toca 511 & Toca FC at the time of surgical resection will be presented at the 2018 American Academy of Neurology (AAN) Annual Meeting and 2018 American Association of Neurological Surgeons (AANS) Annual Scientific Meeting. Previously disclosed clinical data will also be reviewed at these meetings (Press release, Tocagen, APR 17, 2018, View Source;p=RssLanding&cat=news&id=2342917 [SID1234525819]).

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Additionally, preclinical data describing the level of Toca 511 transduction required for an anti-tumor response will be presented at the 14th Annual PEGS: The Essential Protein Engineering Summit.

Details of the presentation at AAN, held April 21-27 in Los Angeles, are as follows. The full presentation will be placed on Tocagen’s website following the presentation.

Presentation Type: Oral presentation (Abstract: 1173)
Title: Toca 511 & Toca FC: Evaluation of durable response rate in the post-resection setting and association with survival in patients with recurrent high grade glioma
Presenter: Timothy Cloughesy, M.D., director of the University of California, Los Angeles, Neuro-Oncology Program
Date and Time: Tuesday, April 24, 2:00 p.m. – 2:12 p.m. PT

Details of the presentation at the AANS Annual Scientific Meeting, held April 28-May 2 in New Orleans, are as follows:

Presentation Type: Oral presentation (Abstract: 615)
Title: Evaluation of durable response rate in the post-resection setting and association with survival in patients with recurrent high grade glioma who received Toca 511 and Toca FC treatment
Presenter: Bob S. Carter, M.D., Ph.D., chief of the Massachusetts General Hospital department of neurosurgery
Date and Time: Tuesday, May 1, 11:32 a.m. – 11:42 a.m. CT

Details of the presentation at PEGS, held April 30-May 4 in Boston, are as follows. The full presentation will be placed on Tocagen’s website following the presentation.

Presentation Type: Oral presentation
Title: Replicating retroviruses for manipulation of the tumor immune ecosystem: preclinical and clinical outcomes
Presenter: Douglas Jolly, Ph.D., executive vice president of research and pharmaceutical development at Tocagen
Date and Time: Tuesday, May 1, 8:30 – 9:00 a.m. ET

About Toca 511 & Toca FC

Tocagen’s lead product candidate is a two-part cancer-selective immunotherapy comprised of an investigational biologic, Toca 511, and an investigational small molecule, Toca FC. Toca 511 is a retroviral replicating vector (RRV) that selectively infects cancer cells and delivers a gene for the enzyme, cytosine deaminase (CD). Through this targeted delivery, infected cancer cells carry the CD gene and produce CD. Toca FC is an orally administered prodrug, 5-fluorocytosine (5-FC), which is converted into an anti-cancer drug, 5-fluorouracil (5-FU), when it encounters CD. 5-FU kills cancer cells and immune-suppressive myeloid cells in the tumor microenvironment resulting in anti-cancer immune activation and subsequent tumor killing.