On April 12, 2022 Molecular Templates, Inc., (Nasdaq: MTEM, "Molecular Templates" or "MTEM") a clinical-stage biopharmaceutical company focused on the discovery and development of proprietary targeted biologic therapeutics, engineered toxin bodies (ETBs), reported that highlights from the six poster presentations on its pipeline programs that were presented at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022, taking place April 8 – April 13, 2022 at the Ernest N. Morial Convention Center in New Orleans, LA (Press release, Molecular Templates, APR 12, 2022, View Source [SID1234612074]). Copies of the posters presented at AACR (Free AACR Whitepaper) can be found in the Investors section of Molecular Templates’ website under Presentations.

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"We believe that ETBs offer novel biology that have the potential to translate into unique clinical outcomes, even against well-explored targets," said Eric Poma, Ph.D., CEO and CSO of Molecular Templates. "We are seeing differentiated pharmacodynamic effects in patients in our Phase I study with MT-6402, our PD-L1 targeting agent, from both that agent’s direct cell-kill effects and its antigen seeding ability. We believe we can leverage this unique biology across other targets such as CTLA-4, TROP-2, and TIGIT."

Poster Title: A Phase 1 Study of MT-6402, a novel Engineered Toxin Body (ETB) targeting PD-L1, in patients with PD-L1 expressing advanced solid tumors

Authors: David R. Spigel, MD; Eugene Ahn, MD, PhD; John D. Powderly, Herbert L. Duvivier, JD, MD; Drew Rasco, MD; Agnes Rethy, MD; Chris Moore, PhD; Amy Yuet, PhD; Angela Georgy, PharmD; Sandra R. Hankins; Swati Khanna, PhD; Joseph D. Dekker, MD; Brian A. Van Tine, MD
Abstract #: 7936

Poster highlights:

Twelve patients with PD-L1+ relapsed/refractory disease have been treated to date across two dose cohorts: 16 mcg/kg (n=6) and 24 mcg/kg (n=6).
Pharmacodynamic (PD) effects including monocyte and myeloid-derived suppressor cell depletion and T cell activation have been observed in the majority of patients. The extent and timing of these PD effects appear dose-related with patients in the 24 mcg/kg cohort generally showing a more rapid and profound PD effect.
One patient in the first cohort with non-small cell lung cancer (NSCLC) (osseous non-measurable disease only) that had progressed after prior checkpoint therapy (PD-1 and CTLA-4) showed qualitative reduction in tumor burden.
One dose-limiting toxicity (DLT) was observed in a single patient (24 mcg/kg). The patient experienced dermatitis that resolved rapidly with systemic steroids. The patient was rechallenged without incident at 24 mcg/kg. No other DLTs have been reported.
Poster Title: Altering tumor immunophenotypes with PD-L1 engineered toxin bodies

Authors: Swati Khanna, Elizabeth M. Kapeel, Lauren R. Byrne, Elizabeth Saputra, Steven Rivera, Lindsey Aschenbach, Lilia A. Rabia, Garrett L. Cornelison, Rachael M. Orlandella, Brigitte Brieschke, Michaela Sousares, Jay Zhao, Garrett L. Robinson, Chris B. Moore, Joseph D. Dekker
Abstract #: 3543

Poster highlights

Molecular Templates’ Antigen Seeding Technology (AST) is a unique approach that allows for specific alteration of tumor immunophenotype to match pre-existing CD8+ T-cells in a patient. This approach is currently being tested clinically with MT-6402, a PD-L1 targeted ETB that delivers an HLA-A2 antigen derived from cytomegalovirus (CMV).
Data are presented here demonstrating that MT-6402 can be altered to present antigens derived from CMV corresponding to other HLA genotypes, thereby broadening the potential patient population that could benefit from this approach.
Poster Title: A CTLA-4-targeted ETB for Treg depletion shows favorable preclinical efficacy and safety

Authors: Asis Sarkar, Rebecca Martin, Lauren R. Byrne, Kiheon Baek, James Pazar, Caleigh Howard, Swati Khanna, Lilia A. Rabia, Diana Adhikari, Michaela M. Sousares, Alvaro Aldana, Abdul G. Khan, Garrett L. Robinson, Jay Zhao, Chris B. Moore, Aimee Iberg
Abstract #: 3538

Poster highlights:

CTLA-4-targeted ETBs are designed to preferentially deplete regulatory T cells (Tregs), via a direct cell kill mechanism of action that is independent of effector cells, in the tumor microenvironment (TME) to improve efficacy and reduce the toxicity associated with CTLA-4 targeted antibodies.
In a transgenic mouse model expressing human CTLA-4 and bearing syngeneic subcutaneous tumors, CTLA-4 ETB treatment depleted Tregs in the TME.
CTLA-4 ETB candidate was well tolerated in a non-human primate toxicology study.
Overall, these preclinical data support the use of ETB technology to deplete immune suppressive regulatory T cells in the TME to allow immune reactivation to tumor.
Poster Title: Engineered Toxin Bodies (ETBs) targeting Trop2​

Authors: Garrett L. Cornelison, Adam Bartos, Brigitte Brieschke, Jessica Momb, Ileana Pedraza, Elizabeth M. Kapeel, Rebecca Martin, Channing Pletka, Adrian Gonzalez, Joseph D. Dekker, Jay Zhao, John Majercak, Garrett L. Robinson.
Abstract: #326

Poster highlights:

Trop2 targeted ETBs show in vitro target specific picomolar potency on Trop2 positive tumor cell lines.
AST enabled Trop2 targeted ETBs to retain direct cell kill potency and alter the tumor immunophenotype to allow for antigen specific T-cell recognition.
Final lead selection based on evaluation of additional targeting domains and AST antigens is underway.
Poster Title: Improving immunotoxin-based therapeutics for cancer with de-immunized Engineered Toxin Bodies

Authors: Rachael M. Orlandella, Elizabeth M. Kapeel, Swati Khanna, Brigitte Brieschke, Garrett L. Robinson, Joseph D. Dekker, and Chris B. Moore
Abstract #: 2579

Poster highlights:

Molecular Templates has developed a de-immunized form of Shiga-like Toxin A (SLTA), incorporated into next-generation ETBs currently in clinical trials, that has demonstrated a lack of innate immune activation and capillary leak syndrome (CLS) in animal models and patients.
Ex vivo assays using peripheral blood mononuclear cells (PBMCs) demonstrate that unmodified SLTA displays upregulation of CCL3, CCL4, TNFα and IL-6, indicating a similar, but not identical, pattern of cytokine release relative to the positive control, lipopolysaccharide (LPS), while the de-immunized SLTA did not activate cytokine or chemokine release.
These data help confirm the observations in animal models and patients that indicate the de-immunized SLTA scaffold lacks the ability to trigger innate immunity seen with unmodified SLTA used in first generation ETBs.
Poster Title: C-KIT/CD117 targeted ETBs for cancer therapy and HSC transplant conditioning

Authors: Caleigh Howard, Shu Wiley, Wenzhao Dong, Andrea Mendiola, Veronica Partridge, Antonio Luz, Sara LeMar, Paul Amador, Amit Kumar Chaudhary, Joseph D. Dekker, Jay Zhao, Ross Durland, Aimee Iberg
Abstract #: 335

Poster highlights:

Molecular Templates has developed CD117 targeting ETBs that may have potential uses in myeloablation or in oncology.
CD117 ETB drug conjugates with MMAF demonstrated increased cytotoxicity compared to stand-alone ETBs or inactive ETB drug conjugate controls and also highlighted the internalization augmenting capabilities of ETBs.

On April 12, 2022 Cyclacel Pharmaceuticals, Inc. (NASDAQ: CYCC, NASDAQ: CYCCP; "Cyclacel" or the "Company"), a biopharmaceutical company developing innovative medicines based on cancer cell biology, reported a publication in the journal Leukemia titled "Cyclin-dependent kinase inhibitor fadraciclib (CYC065) depletes anti-apoptotic protein and synergizes with venetoclax in primary chronic lymphocytic leukemia cells" (Press release, Cyclacel, APR 12, 2022, View Source [SID1234612071]). Fadraciclib is Cyclacel’s novel CDK2/9 inhibitor, currently in two Phase 1/2 trials, one for the treatment of advanced solid tumors and lymphomas and another for hematological malignancies, including patients with leukemia being treated in combination with venetoclax.

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"Results from this research provide further mechanistic evidence in support of our ongoing Phase 1/2 clinical study of oral fadraciclib in select hematological malignancies," said Mark Kirschbaum, M.D., Senior Vice President and Chief Medical Officer of Cyclacel. "The findings confirmed that fadraciclib suppresses MCL1 and synergizes with venetoclax, the only FDA-approved apoptosis enabling leukemia treatment. We have included a cohort within the proof-of-concept part of our Phase 1/2 study that will evaluate the combination of fadraciclib plus venetoclax in patients who have previously failed venetoclax-based regimens."

Researchers from the Department of Experimental Therapeutics and the Department of Leukemia at The University of Texas MD Anderson Cancer Center published preclinical data interrogating fadraciclib’s mechanism of action against primary cell lines of chronic lymphocytic leukemia (CLL), both as a single agent and in combination with the BCL2 antagonist, venetoclax.

Results from the study confirmed that fadraciclib inhibited CDK9 mediated transcription, reduced levels of the short-lived anti-apoptotic protein MCL1, and induced apoptosis in primary CLL cells. The data highlighted the importance of continuous treatment to prevent recovery of MCL1 protein levels. Fadraciclib is the only transcriptional CDK inhibitor in clinical development that is being dosed on a daily schedule by mouth.

Fadraciclib was shown to combine synergistically with venetoclax, the only FDA-approved apoptosis enabling, leukemia treatment. Furthermore, it was demonstrated that the best synergy, with fadraciclib and venetoclax given at the same time, was achieved in 17p deleted CLL cells, which were not sensitive to either agent alone.

Fadraciclib also overcame protection mediated by stroma CLL cells and lymph node microenvironment. This may be important for clinical translation as venetoclax appears to be less effective in the lymph nodes.1

The data support the rationale for pursuing clinical development of fadraciclib, either alone or in combination with a BCL2 antagonist, for the treatment of CLL.

Phase 1/2 Study in Hematological Malignancies (065-102; NCT#05168904)
A Phase 1/2 registration-directed trial, testing oral fadraciclib in various hematological malignancies is currently enrolling patients. The trial uses a streamlined design and will determine the recommended Phase 2 dose (RP2D) for single-agent, oral fadraciclib and then enter into proof-of-concept, cohort stage, using a Simon 2-stage design, where fadraciclib will be administered, both as a single agent and in combinations, to patients in up to seven cohorts relevant to the drug’s mechanism of action and informed by the clinical activity of fadraciclib in previous studies.

Single-agent cohorts will include patients with acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS) who have an inadequate response or have progressed on venetoclax combinations with hypomethylating agent (HMA) or low dose Ara C; relapsed/refractory AML or MDS patients with FLT3, KIT or MAPK pathways (including N and K RAS, BRAF, PTPN11, NF1). The trial will also include patients with CLL who have progressed after at least two lines of therapy including a BTK inhibitor and/or venetoclax.

Combination cohorts for patients with AML or MDS include: fadraciclib and azacitidine for patients with AML or MDS who progressed after hypomethylating agent (HMA) therapy and also fadraciclib and venetoclax for patients that have progressed after venetoclax therapy. Another combination cohort of fadraciclib and venetoclax will enroll patients with CLL or small lymphocytic lymphoma (SLL) who have progressed after venetoclax based regimens. An additional basket cohort will evaluate patients with biomarkers relevant to the drug’s mechanism, including MCL1 and MYC.

Phase 1/2 Study in Advanced Solid Tumors and Lymphomas (065-101; NCT#04983810)
In this ongoing study of fadraciclib 12 patients have been treated in four dose escalation levels. The proof-of-concept stage includes 7 histologically defined cohorts thought to be sensitive to the drug’s mechanism: breast, colorectal (including KRAS mutant), endometrial/ uterine, hepatobiliary, ovarian cancers and lymphomas. An additional basket cohort will enroll patients regardless of histology with biomarkers relevant to the drug’s mechanism, including MCL1, MYC and/or cyclin E amplified.

About Cyclin-Dependent Kinases and Fadraciclib
Cyclin-dependent kinases (CDKs) are critical for cell cycle control and transcriptional regulation. Dysregulated CDKs have been linked to the cancer hallmarks of uncontrolled proliferation and increased cancer cell survival. Fadraciclib, a next generation CDK inhibitor, is a highly selective, potent, orally and intravenously available, inhibitor of CDK2 and CDK9. CDK2 drives cell cycle transitions and CDK9 regulates transcription of genes through phosphorylation of the carboxy-terminal domain (CTD) of RNA polymerase II (RNAP II). By inhibiting CDK2 and CDK9 fadraciclib causes apoptotic death of cancer cells at sub-micromolar concentrations. Published data support the hypothesis that concomitant inhibition of CDK2 and CDK9 yields synergistic anti-tumor activity rather than inhibition of CDK2 or CDK9 alone.

Preclinical and animal model data suggest that fadraciclib may benefit patients with adult and pediatric hematological malignancies, such as ALL, AML, B-cell lymphoma, CLL, and multiple myeloma and certain cyclin E-addicted or MYC-amplified solid tumors, including certain forms of breast cancer, neuroblastoma, ovarian cancer and uterine serous carcinoma. Similarly to FDA-approved CDK4/6 inhibitors, fadraciclib may be useful in combination with other anticancer drugs, including HER2 inhibitors, such as trastuzumab, or BCL2 inhibitors, such as venetoclax.

Venetoclax has modest single-agent activity in AML. MCL1 dependence appears to correlate with resistance to venetoclax. Preclinical data have confirmed synergy of fadraciclib and venetoclax, suggesting that the suppression of both BCL2 and MCL1 may be more beneficial than inhibiting either protein alone. Pre-existing or emergent mutations in the MAPK pathway contribute towards resistance to venetoclax, FLT3 inhibitors and mutant IDH inhibitors. These mutations are also frequent in proliferative CMML progressing to AML. Activating mutations in the MAPK pathway upregulates MCL1 and renders AML resistant to apoptosis. CDK9 inhibition downregulates MCL1 transcriptionally and can potentially be effective in the context of MAPK and other receptor tyrosine kinase mutations.

In a prior Phase 1 open-label trial (CYC065-01), patients with high copy CCNE (cyclin E), MYC or MCL1 showed sensitivity to intravenously administered, single-agent fadraciclib. A heavily pretreated patient with MCL1 amplified endometrial cancer achieved a radiographically confirmed partial response (PR) after a month and a half on fadraciclib. This patient continues on therapy for over two years and reduction in her target tumor lesions has reached 100%. An additional patient with cyclin E amplified ovarian cancer achieved stable disease with 29% shrinkage in her target tumor lesions.2

On April 12, 2022 PerkinElmer, Inc. (NYSE: PKI), a global leader committed to innovating for a healthier world, reported that the Company will release its first quarter 2022 financial results after market close on Tuesday, May 3, 2022 (Press release, PerkinElmer, APR 12, 2022, View Source [SID1234612069]). The Company will host a conference call the same day at 5:00 p.m. ET to discuss these results. Prahlad Singh, president and chief executive officer, and Jamey Mock, senior vice president and chief financial officer, will host the conference call.

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To access the call, a live audio webcast will be available via this registration form or on the Investors section of the Company’s website.

A replay of the webcast will be available beginning at 7:00 p.m. ET, Tuesday, May 3, 2022 through the Investors section of the Company’s website.

On April 12, 2022 Pathios Therapeutics Limited ("Pathios"), a biotech company focused on the development of first-in-class therapies for cancer, reported that new data on PTT-3213, the company’s orally bioavailable, potent and selective GPR65 inhibitor, were reported in a podium presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022 (Press release, Pathios Therapeutics, APR 12, 2022, View Source [SID1234612068]). Presented findings from human genetic and ex vivo human cellular studies demonstrated that GPR65, a pH-sensing, G protein-coupled receptor, serves as a critical innate immune checkpoint in the human tumor microenvironment. Furthermore, data showed that inhibition of GPR65 with PTT-3213 resulted in significantly reduced tumor growth in the MC38 mouse syngeneic cancer model. The AACR (Free AACR Whitepaper) conference is being held April 8-13, 2022 in New Orleans, Louisiana.

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Stuart Hughes, Ph.D., Pathios’ chief executive officer, delivered the podium presentation as part of the conference’s "Cancer Biology and Tumor Immunity" mini-symposium. The key findings presented included:

In response to acidic pH, human macrophages undergo profound alterations in gene expression that render them indistinguishable from a typical immunosuppressive tumor associated macrophage. Pathios’ small molecule GPR65 inhibitors are able to fully counteract this polarization and re-establish an anti-tumorigenic phenotype
In vivo studies in the MC38 colon cancer syngeneic mouse model demonstrated that once weekly oral dosing with PTT-32131 provided equivalent efficacy to dosing twice weekly with a murine anti-PD-1 antibody
The combination of PTT-3213 and anti-PD-1 therapy provided greater efficacy than either agent gave alone in the MC38 colon cancer syngeneic mouse model
Inhibition of GPR65 by PTT-3213 was associated with significant increases in tumor-infiltrating CD8+ T cells and natural killer T (NKT) cells, both cell types with critical tumor cell killing capabilities. There was a clear correlation between the increased infiltration of these cells and decreased tumor volume across combination groups
"These are powerful findings as they firmly demonstrate the substantial clinical promise of GPR65 inhibition as a novel immuno-oncology strategy in a range of solid cancers. Importantly, these data further validate our long-held view that low pH acting on GPR65 is a critical innate immune checkpoint and the key determinant of immunosuppressive myeloid cells in the tumor microenvironment," commented Dr. Hughes. "As highlighted during our AACR (Free AACR Whitepaper) presentation, we have now assembled a robust collection of data on the associations between the human genetics of GPR65 and cancer outcomes, including ex vivo studies in human cells. Additionally, we have now shown that weekly dosing of a small molecule GPR65 inhibitor is able to provide equivalent efficacy to anti-PD-1. We look forward to continuing research into this novel immuno-oncology target as we build on this data and complete further candidate nomination studies through 2022."

About Acidity in the Tumor Microenvironment

The acidic tumor microenvironment, inherent to many cancers, causes a profound immunosuppression of infiltrating immune cells. This environment disarms the anti-cancer immune response and negates the effectiveness of current immunotherapies. This is particularly evident in tumor associated macrophages (TAM), where acidity is sensed by the cell-surface receptor GPR65, leading to an induction of the transcriptional repressor ICER (inducible cAMP early repressor) and the widespread suppression of a host of pro-inflammatory mediators and anti-tumorigenic genes.

On April 12, 2022 Panbela Therapeutics, Inc. (Nasdaq: PBLA), a clinical stage biopharmaceutical company developing disruptive therapeutics for the treatment of patients with cancer reported a poster presentation highlighting the results for SBP-101 as a polyamine metabolism modulator in ovarian cancer at the American Association for Cancer Research (AACR) (Free AACR Whitepaper), taking place April 8-13, 2022 (Press release, Panbela Therapeutics, APR 12, 2022, View Source;utm_medium=rss&utm_campaign=panbela-announces-poster-presentation-at-american-association-for-cancer-research [SID1234612067]). The work reflects the Company’s ongoing collaboration with Johns Hopkins University School of Medicine.

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"The treatment of C57Bl/6 mice injected with VDID8+ ovarian cancer with SBP-101 was observed to significantly prolong survival and decrease overall tumor burden," said Jennifer K. Simpson, PhD, MSN, CRNP, President & Chief Executive Officer of Panbela. "We are grateful to our collaborators at Johns Hopkins University School of Medicine, who are on the leading edge of cancer research. This data supports our efforts to initiate an ovarian cancer program this year. Additionally, we are excited to review these results on an R&D call planned for May 3, 9:00 AM EST."

"The results suggest that SBP-101 may have a role in the clinical management of ovarian cancer," said Dr. Simpson, "We look forward to continuing our studies in ovarian, and other cancers, to develop effective therapeutics for patients with unmet medical needs."

The poster highlights the role of naturally occurring polyamines, putrescine, spermidine and spermine, as essential for cellular growth and proliferation. As such, many cancers are reliant on elevated polyamine levels that are maintained through dysregulated polyamine metabolism. Polyamine metabolism is thus a promising target for cancer therapeutics, and modulation of polyamine metabolism has been attempted with numerous enzyme inhibitors and polyamine analogues. SBP-101 (diethyl dihydroxyhomospermine) is a novel spermine analogue that has shown efficacy in slowing pancreatic tumor progression both in vitro and in vivo.

This study determined the effect of SBP-101 treatment on polyamine metabolism in a variety of cancer cell types in vitro including lung, ovarian, prostate, pancreatic and breast. In addition, the activity of four enzymes involved in the polyamine pathway following treatment with either SBP-101 or the well-characterized spermine analogue, BENSpm (N1,N11-bisethylnorspermine) was evaluated. These results indicate that SBP-101 likely exerts its effects predominately through decreased polyamine biosynthesis with minor upregulation of catabolism, in contrast to the structurally similar BENSpm where the increase in polyamine catabolism is the predominant response.

The efficacy of SBP-101 utilizing the VDID8+ murine ovarian cancer model (ID8+ C57Bl/6 ovarian cells overexpressing both VEGF and Defensin) was evaluated. The mice were treated with SBP-101 at either 24 mg/kg or 6 mg/kg alternating MWF. Both doses of SBP-101 produced a statistically significant prolongation of survival (24mg/kg p=.0049, 6 mg/kg p=.0042). There was no significant difference in response between the two SBP-101 doses. The prolonged survival was correlated with a delay in the production of ascites, the indication of tumor burden in this model. Additionally, when SBP-101 treated mice succumbed to the disease, their overall tumor burden was lower when compared to control mice.

The poster concludes that the treatment of C57Bl/6 mice injected with VDID8+ ovarian cancer with SBP-101 significantly prolonged survival and decreased overall tumor burden. Future studies will be designed to evaluate the effects of SBP-101 in combination with other polyamine metabolism modulators as well as with immune modulators.

Details of the presentation are as follows:

Poster Presentation

Title: The potential of spermine analogue SBP-101 (diethyl dihydroxyhomospermine) as a polyamine metabolism modulator in ovarian cancer
Session Category: Experimental and Molecular Therapeutics
Session Title: Small Molecule Therapeutic Agents Abstract #: 5488

Additional meeting information can be found on the AACR (Free AACR Whitepaper) website: Abstracts | AACR (Free AACR Whitepaper) Annual Meeting 2022 | April 8-13, 2022 | New Orleans

The poster will also be available on the Company’s website at View Source .

About SBP-101

SBP-101 is a proprietary polyamine analogue designed to induce polyamine metabolic inhibition (PMI) by exploiting an observed high affinity of the compound for pancreatic ductal adenocarcinoma and other tumors. The molecule has shown signals of tumor growth inhibition in clinical studies of US and Australian metastatic pancreatic cancer patients, demonstrating a median overall survival (OS) of 12.0 months which is not yet final, and an objective response rate (ORR) of 48%, both exceeding what is seen typically with the standard of care of gemcitabine + nab-paclitaxel suggesting potential complementary activity with the existing FDA-approved standard chemotherapy regimen. In data evaluated from clinical studies to date, SBP-101 has not shown exacerbation of bone marrow suppression and peripheral neuropathy, which can be chemotherapy-related adverse events. Serious visual adverse events have been evaluated and patients with a history of retinopathy or at risk of retinal detachment will be excluded from future SBP-101 studies. The safety data and PMI profile observed in the current Panbela sponsored clinical trial provides support for continued evaluation of SBP-101 in a randomized clinical trial. For more information, please visit View Source .