Vincerx Pharma, Inc.
Last update: February 18, 2022 9:00 ET
CONTENTSCapital Structure Background & Management Ownership Clinical Candidates Competition Pre-clinical Pipeline Patents Bayer License Agreement Upcoming Milestones
|VINC US Equity||in millions
|Price per share||5.96||Feb 18, 2022|
|Shares outstanding||21||End Q3 2021|
Background & Management
Vincerx Pharma was founded by CEO Ahmed Hamdy, MD, COO Raquel Izumi, PhD, CBO Stuart Hwang, PhD, General Counsel, Tom Thomas and John Byrd, MD. The SPAC, Lifesci investments (founding Partner: Andrew I. McDonald, Ph.D), led Vincerx’s NASDAQ listing after consummation of a merger agreement on December 23, 2020.
Ahmed and Raquel have a strong record in the industry. They co-founded Acerta Pharma in 2013 and developed BTK inhibitor, acalabrutinib (now Calquence, $511 M annual US revenue, 20201). Three years after inception, Acerta Pharma was brought under the control of AstraZeneca after a majority equity investment in Q1 of 2016. (55% of shares purchased for $2.5 billion in cash + $1.5 billion unconditional payment on first regulatory approval of acalabrutinib/at end of 2018).
Prior to founding Acerta, Ahmed led Pharmacyclics as CMO (2008 to 2011) leading development of another BTK inhibitor, ibrutinib. Ahmed was responsible for taking ibrunitib from a pre-clinical stage into phase II. Overlapping his tenure from 2010 to 2011 was Raquel as Senior Director of Clinical Development. Pharmacyclics was able to cut a $975 M partnership deal with Janssen ($150 M upfront + $825 M development+regulatory milestone payments + 40/60 development cost share + 50/50 P/L share). The company was later acquired by AbbVie in 2015 for $21 billion in one of the largest biopharma M&A deals to date.
The Vincerx management is shrewd and well-acquainted with regulatory affairs and the FDA's accelerated approval program. At Acerta, Ahmed and Raquel took acalabrutinib as a preclinical asset in 2013 (at founding of company) to treating MCL patients commercially in 2017. At Pharmacyclics, Ahmed was responsible for developing ibrutinib from its pre-clinical stage through to phase II. This was done in under 3 years, with all three phase II studies gaining Breakthrough Therapy Designation from the FDA and paths to accelerated approval.
Vice President Clinical Operations at Vincerx, Tasheda Navarro was also in Acerta (2014-2020) and Pharmacyclics (2010-2012) as Senior Director of Clinical Operations and Senior Clinical Trial Manager in the two companies respectively. At Pharmacyclics she managed the phase II ibrutinib trial in CLL leading to its accelerated approval in 2014 and at Acerta she led clinical operations of the CLL program for acalabrutinib.
In March 2021, Vincera announced three new appointments to its management team.
Hermes Garbán, M.D., Ph.D, prior Head, Therapeutics Discovery and Development at ImmunityBio (NASDAQ:IBRX, 2019-2021) who will serve as CMO.
Hans-Georg Lerchen, Ph.D. will join as CSO. I believe Hans-Georg is going to be a key driver of the medium-long term value of the company. He was a Distinguished Fellow in the Bayer Science Fellow Network in the Pharmaceuticals division of Bayer. At Bayer he led the development of ADCs with KSP inhibitors using the legumain linker platform. He has also worked on camptothecin glycoconjugates. The assets stemming from these programs were acquired by Vincerx and make up the large part of the company's pre-clinical pipeline. He is first author on a paper published in Angewandte Chemie, International Edition in 2018 - Antibody-Drug Conjugates with Pyrrole-Based KSP Inhibitors as the Payload Class, as discussed below.
Ownership (last update: Feb 18 2021)
The management team has lots of skin in the game. Ahmed, Raquel and Chair of Scientific Advisory Board John Byrd each own over 1.6 M shares each representing ~23% of the company. Each of these three are entitled to receive an additional 1,765,308 earnout shares on the condition of stock performance.
Other notable owners of the company: Rubric Capital Management (10% of total shares outstanding), Affinity Asset Advisors (5.4%, purchased an additional 130,365 shares in Q4 2021), Holocene Advisors (3.6%).
|Name||Shares||% of total|
|Rubric Capital Management||2,107,000||10.0%|
|CEO Ahmed Hamdy||1,632,479||7.8%|
|COO Raquel Izumi||1,619,199||7.7%|
|John C. Byrd, SAB||1,618,199||7.7%|
|Sage Rhino Capital||1,618,199||7.7%|
|Deerfield Management Company||1,379,310||6.6%|
|Tang Capital Partners||1,030,634||4.9%|
|Andrew McDonald (BoD)||808,471||3.8%|
|Rock Springs Capital Management||800,295||3.8%|
|Sphera Funds Management||720,161||3.4%|
|Point72 Asset Management||344,827||1.6%|
|TOTAL OF LISTED||17,712,049||84%|
|Candidate||Mechanism of Action||Indication||Phase|
|VIP152||PTEFb/CDK9 inhibitor - IV||Myc-driven NHL, solid tumors, CLL, RS||Ib|
|VIP236||αvβ3 integrin antagonist-camptothecin derivative conjugate||Solid tumors||IND:2H22|
|VIP943||Anti-CD123 ADC (KSP inhibitor)||Leukemias, MDS||Preclin|
|VIP924||Anti-CXCR5 ADC (KSP inhibitor)||B-cell malignancies||Preclin|
|VIP217||PTEFb/CDK9 inhibitor - Oral||Oral follow-on||Disc|
VIP152 (formerly known as BAY 1251152)
VIP152 is the company's lead candidate, a highly selective P-TEFb (CDK9) inhibitor discovered at Bayer. P-TEFb (positive transcription elongation factor beta) is a protein complex comprising CDK9 and a cyclin binding partner (T1, T2A/B or K). When active, it phosphorylates the C-terminal domain of RNA polymerase II and elongation factor DSIF leading to release of the promoter pause and transcriptional elongation2. Target genes of active P-TEFb include anti-apoptotic genes such as MYC, MCL1, and others. Aberrant P-TEFb activity leads to overexpression of these genes, which play a large factor in tumor survival and resistance to treatment. VIP152 inhibits P-TEFb's phosphorylation activity with an IC50 of 3-4 nM (low and high ATP). It has high in-vitro selectivity over other CDK family members. The median IC50 in a panel of 33 tumor cell lines was 67 nM (proliferation inhibition, as reported in SEC filings). The drug is currently being tested in Phase I expansion cohorts (NCT02635672) with patients required to either have Myc-aberrated r/r aggressive lymphoma (Arm 1) or Myc-abberated advanced solid tumors (Arm 2). Note that all patients must have confirmed MYC overexpression or translocation. The first patient was dosed on June 3 2021. A second trial (NCT04978779) in CLL and Richter Syndrome (RS) patients r/r to venetoclax and/or ibrutinib with a requirement for MYC-aberration is also underway, with the first patient dosed on December 17 2021. After dose escalation, the company intends to enroll 20 additional patients in each of the CLL and RS cohorts. The company is on track to initiate potential Phase 2 studies in the second half of 2022, as monotherapy and in combination with Pembrolizumab.
VIP152 - clinical data
The company is focusing on patients who are most likely to respond to CDK9 inhibitor treatment - those with MYC aberrations and those who have failed BTK and/or Venetoclax treatment where the highest unmet medical need lies.
Prior Phase 1 (NCT02635672) data released were very compelling. They enrolled 31 patients (all-comer advanced cancer with no biomarker selection), 97% of which had prior systemic chemotherapies. From 7 'double-hit' (DH) DLBCL, they had 2 PET-negative CRs (complete metabolic remissions). Both CRs have had significant duration with one patient on treatment for 3.6 years and the other for 2.3 years. These patients ended treatment due to the COVID pandemic but have remained in remission as of December 2021.
Of the total 31 treated patients, there were no major treatment-related SAEs. No patients withdrew due to toxicity. There were 9 cases of Grade 3/4 neutropenia and 3 cases of Grade 3 anemia. Early neutropenia observed in the trial indicates an on-target effect of MCL1 downregulation and pharmacodynamic evidence of the drug working. The neutropenia was manageable (with dose reductions and/or growth factor support), and it is worthy to note that no patients dropped out of the study due to toxicity. There have been no major unexpected adverse events in the two patients with CRs, highlighting a favorable tolerability profile in the context of extended treatment.
A paper published in Clinical Cancer Research in February 2022 (access here) highlighted Phase I (NCT02635672) data from 37 patients who received more than 1 dose of VIP152. 24 of these patients had had ≥3 prior systemic therapies (65%). The MTD identified was 30 mg, limited largely by on-target-related neutropenia. The two CRs observed in high-grade lymphoma (DH-DLBCL) were in patients treated with the 30 mg once-weekly dose. Of 30 solid tumor patients treated in the dose escalation (unselected patients), there were 7 cases of stable disease, 5 of whom received either 22.5 or 30 mg. Two notable long-duration cases of SD occured in a patient with pancreatic cancer and another with salivary gland cancer (9.5 and 16.8 months respectively).
Double-hit lymphoma (DHL)
This is a genetic subtype of DLBCL with concurrent chromosomal rearrangements affecting MYC and BCL2 (or BCL6). These are aggressive lymphomas associated with poor prognosis and represent 5-11% of DLBCL patients.3,4The strong responses seen in these patients in the Phase 1 trial serve as the basis for trialling the drug in other MYC-aberrated cancers.
Double expressor lymphomas (DEL)
These are lymphomas that do not have MYC/BCL2(or BCL6) chromosomal rearrangements but have concurrent expression of MYC and BCL-2. This is seen in 21-29%3,5 of patients and is also associated with poor prognosis under current treatment protocols.
From preclinical xenograft data shared by the company, clear reductions were seen in MYC and MCL1 expression.
Similar data was observed in patient samples from the phase I trial, showing marked reductions in MYC and MCL1 mRNA. Note that the biological half-life of the drug is 4 hours.
Inhibition of CDK9 drastically reduces MCL-1 expression. The upregulation of MCL-1 is known to be a huge contributing factor to chemoresistance in r/r patients, and is especially the case where patients fail to respond to the BH3-mimetic/Bcl-2 inhibitor venetoclax. As a result, the relapsed/refractory population is enriched with MYC and MCL-1 overexpressing lymphomas.
There is an opportunity here for synergy with Bcl-2 inhibition, with a CDK9 inhibitor potentially making otherwise chemo-resistant cells sensitive to Bcl-2 inhibition again. This could be true especially where BAK/BAX have been sequestered by a flood of MCL-1 which have halted apoptosis. By reducing MCL-1 expression, this mode of sequestration is curtailed, and the cell may be re-sensitized to Bcl-2 inhibition at therapeutic doses. 6 This is not to say that MCL-1 depletion on its own will likely be sufficient to induce apoptosis.
A competing CDK9 inhibitor from AstraZeneca, AZD4573, currently in Ph1/2, has also demonstrated very compelling pre-clinical data with similar apoptosis-inducing effects in a wide range of cancer cell lines. The combination of AZD4573 with venetoclax produced highly durable regressions in an OCI-AML3 subcutaneous xenograft model, which otherwise did not respond to venetoclax or AZD4573 monotherapy7. In OCI-AML3 cells treated with venetoclax alone, co-imunoprecipitation with anti-MCL-1 and anti-BID antibodies indicated Bim displacing from Bcl-2 and being sequestered by MCL-1, creating an MCL-1 dependence that may be counteracted by MCL-1 downregulation. Hence, the combination of Bcl-2 inhibition with MCL-1 downregulation has great potential.
Synthetic Lethality in combination with EIF2 signalling inhibitionPre-clinical data presented at ASH 2021 (video presentation) indicated a potential for synthetic lethal combinations with VIP152, particularly with the inhibition of EIF2 signalling. This could potentially be accomplished with low doses of a PERK inhibitor, such as GSK's GSK2606414 which has otherwise been limited by pancreatic toxicity19.
Opportunities in other indications
Myc is amplified in up to 50% of all tumors. (Sarah Cannon Network Data). It is a well-known oncogene that has been hard to target due to its lacking of a specific active site. However, as shown in the pre-clinical data above, CDK9 inhibition such as that through VIP152 dramatically reduces MYC mRNA and can serve as a proxy for Myc inhibition. The company is planning to test VIP152 in various solid tumors such as Ovarian, TNBC, CRPC-NE where patients are required to have diagnostically identified MYC aberrations.
The most advanced CDK inhibitor in the clinic that also targets CDK9 is alvocidib (flavopiridol) being developed by Tolero (acquired by Sumitomo Dainippon Pharma Oncology), although this is more a pan-CDK inhibitor, targeting CDK1, 2, 4, 6 and 9, all in the 20-60 nM range. It has a therapeutic index of less than 1.8 They are in Phase 2 for AML (as monotherapy or in combination with chemo) and MDS. They also have a collaboration with AbbVie for a combination trial with venetoclax in AML. Strikingly, a biomarker-driven Phase II study of alvocidib in combination with cytarabine and mitoxantrone in newly diagnosed and r/r MCL-dependent AML resulted in 8/13 (62%) CR/CRi. The data were presented at ASH 2020 here. The drug has since been discontinued, however a prodrug of alvocidib, TP-1287 is currently being developed by Sumitomo Dainippon with a Phase I trial currently recruiting patients.
Fadraciclib (CYC065), being developed by Cyclacel Pharmaceuticals is a CDK2/9 inhibitor that recently reported Phase I data at the 2020 EORTC-NCI-AACR (ENA) Symposium. From 21 IV-treated patients, one with MCL1-amplified endometrial cancer had a PR after 6 weeks on drug. The patient had failed 7 prior lines of therapy and has continued treatment for 18+ months with 96% reduction in tumor lesions. They have since enrolled 19 patients with r/r AML/MDS in combination with venetoclax and plan to release data in this cohort this year.
Zotiraciclib (TG02), is a multi-kinase inhibitor being developed by Adastra Pharmaceuticals and entering a registratio-enabling study for GBM patients in 1H21 based on this published data. While it can potently inhibit CDK9 (IC50: 3 nM), it also inhibits CDK1,2,3,5 with IC50s all in the 3-9 nM range and JAK2, TYK2, ERK7, ERK5, FLT3 from 14-43 nM.
The most famous/successful of CDK9+ inhibitors is dinaciclib, (CDK1,2,5,9 IC50: 1-40 nM). It was brought to phase III in 2012 by Merck in a head-to-head against ofatunumab. The trial was going to enrol 284-466 r/r CLL patients but was terminated early when Merck decided to prioritise development of pembrolizumab. Of the patients treated in this trial however, a 2017 publication in Blood revealed an ORR of 40% (8/20) in dinaciclib-treated patients vs 8.3% (2/24) in ofatumumab-treated patients. The median PFS was 13.7 months (dinaciclib) vs 5.9 months (ofatumumab). These were patients with a median 3 prior lines of therapy. Clinical development of dinaciclib has not been pursued since, and with its COM patent (US: 7,119,200, filed 2004) expiring soon, I don't think Merck is going to be picking the program up again at this point. However, it is interesting to note that a method-of-use patent regarding dinaciclib (US: 9925192) was filed in 2015 to treat cancer with a venetoclax-dinaciclib combination. In this patent they showed huge synergistic effects with dinaciclib/venetoclax combination treatment in SCLC and DLBCL xenograft tumor models.
In addition to this, an article published just this month in Nature Scientific Reports highlighted CDK9 inhibition specifically as the main source of dinaciclib's apoptotic effects, with MCL-1 downregulation playing a major role. They used medulloblastoma cells and also saw synergistic effects when BH3 mimetics were combined with dinaciclib, giving more credence to the potential of venetoclax-CDK9 inhibitor combinations.
AstraZeneca's AZD4573 has a 10-fold selectivity over 13/14 other kinases tested. It is in phase I/II. Kronos Bio has CDK9-selective inhibitor, KB-0742, and began recruiting for its phase I in Q1 of this year. They are looking at any r/r solid tumors or NHL and plan to report initial safety, PK and PD data from dose escalation cohorts in Q4. Prelude Therapeutics has PRT2527. They are planning to file an IND sometime this year.
Vincerx has an intriguing pre-clinical pipeline. With recent hire of former Bayer medicinal chemist, Hans-Georg Lerchen, I believe the company is moving in the right trajectory to deliver on these assets.
VIP236 - Small Molecule Drug Bioconjugate
This is the company's leading pre-clinical candidate with an IND filing on track for the second half of 2022. Its novel mechanism of action was recently revealed in the AACR 2021 abstract (no.1314). It is an αvβ3 integrin antagonist linked to a cytotoxic camptothecin derivative via a linker that is cleaved by neutrophil elastase (tumor-stroma associated). The αvβ3 integrin is overexpressed on tumor cells and angiogenic blood vessels (as in the case with tumor-associated vasculature).
Imaging data in a mouse model showed a 10-fold increase of the drug in the tumor stroma versus plasma, indicating targeting of cancer cells expressing αvβ3 integrin. The company has reported high efficacy in TNBC, SCLC, RCC and CRC xenograft models.
A paper was published in January 2022 highlighting this data and more, and can be accessed here. As expected, conjugation of the payload to the αvβ3 integrin via a tumor-specific cleavable linker resulted in higher tumor-to-plasma ratios, marked anti-tumor efficacy and favorable tolerability in xenograft models.
Targeting of αv/αvβ3 integrins
Note that the following drugs do not share the mechanism of action of VIP236 but can reveal potential systemic toxicities associated with binding of the αv/αvβ3 integrin. Etaracizumab (MedImmune) is a very old anti-αvβ3 integrin mAb that went through a randomised open-label phase 2 study in metastatic melanoma. Its results are published here. The results of the phase I study can be found here. Overall, there were no significant toxicities associated with the drug, however, clinical response was lacklustre (probably due to weak apoptosis-inducing effects), and its development was discontinued.
Intetumumab (Centocor) is another anti-αv-integrin mAb that was discontinued after failing to show efficacy in a Phase II trial for metastatic melanoma.9
Cilengitide (Merck) is a small molecule selective for αv integrins. It was discontinued after failing to meet its primary endpoint in a Phase III trial for glioblastoma.10
To my knowledge, there have been no antibody or small molecule drug conjugates in the clinic that have used an αvβ3 integrin targeting moiety. In the literature however, the Cochran lab at Stanford has worked on a "knottin–Fc–drug conjugate" with an αv integrin targeting moiety (targeting both αvβ3 and α5β1). They used this to deliver the auristatin tubulin inhibitor MMAF as a payload and showed significant tumor regression in tumor xenograft models with high αv expression (specifically the U87MG tumor cell line, expressing huge amounts of αvβ3 integrin.11,12 The papers were published in 2016.
Camptothecin in the clinic
Camptothecin is a topoisomerase I inhibitor (a key enzyme in DNA replication and repair). CSO Hans-Georg Lerchen is first author on a paper published in 2001 on the design and optimisation of camptothecin glycoconjugates13. The product of this work, BAY 56-3722, moved into a phase II study as a systemic therapy in patients with r/r metastatic CRC14. It was put on clinical hold from excessive toxicity seen in separate studies with HCC patients, and the drug was discontinued altogether by Bayer.
Irinotecan - an old camptothecin derivative approved for metastatic colon cancer and metastatic rectal cancer. It is typically used in combination with 5-FU and LV as 1L therapy. The active metabolite of irinotecan is SN38, which VIP236 is a derivative of.
Belotecan - camptothecin analogue indicated for SCLC and ovarian cancer in South Korea.
Due to their systemic nature, these drugs have various off-target effects. A large number of Grade 3/4 events are observed in the clinic. Clinical trials have shown neutropenia, diarrhea and leukopenia as major drug-related AEs.15
VIP126 - a derivative of SN38, optimised for higher cell membrane permeability and reduced efflux.
VIP236 - SMDC linker
Attached to the hydroxy lactone ring of VIP126. The linker is cleaved by neutrophil elastase to be released in the tumor microenvironment. A necessary component of the drug to prevent the release of active payload in healthy tissues for increased selectivity and reduced off-target effects.
VIP236 - Toxicology & Future
The company has said that preliminary toxicology results have shown that the drug is well-tolerated after repeated dosing in xenograft models. They have generated in vivo proof of concept in multiple solid tumor types (colon, breast, SCLC and RC). The AACR abstract released states tumor growth inhibition seen in xenograft models SW480 (colon cancer), MX1 (breast cancer), and NCI-H69 (lung cancer) with T/C ratios of 0.1, 0.03 and 0.06 (p-value less than 0.05 each, compared to vehicle control) respectively.
The company is planning to file an IND within a year and are planning to initiate a first in human study in multiple solid tumors sometime in 1H22. The company has also said that a publication will be coming out soon on this drug.
VIP943 & VIP924 - Antibody-Drug Conjugate platform
Vincerx has two ADCs using a KSP (kinesin spindle protein) inhibitor as a payload.
VIP943 (f.k.a BAY-943) - targeted to CD123, for leukemias (AML, CML, T-ALL, B-ALL, MDS) with an IND targeted in 18-36 months.
VIP924 (f.k.a BAY-924) - targeted to CXCR5, with an IND targeted in 24-36 months.
History of KSP inhibition
Array BioPharma had a KSP inhibitor, ARRY-520 (filanesib), but it was not conjugated to anything and was discontinued in February 2020, citing inefficacy. Interestingly, Array believed from pre-clinical work 16 that there was a direct relation between MCL-1 expression, cellular MCL-1 dependence and KSP-inhibition-induced-apoptosis by their drug. It was thought that MCL-1-dependent cells that rapidly degrade MCL-1 during mitotic arrest were more likely to be responsive to KSP inhibition by their drug versus cells that depend on the more stable BCL-2/BCL-XL for survival. Stemming from this, they tested the drug in r/r AML and advanced MDS. Note that this was a systemic therapy given over short infusional schedules with a clinical half-life up to 2 days.
Another KSP inhibitor, ispinesib (SB-715992) went through multiple phase I/II trials in HCC, melanoma HNSCC and breast cancer, however efficacy was lacklustre at the doses tested. 17,18
As a payload in an ADC construct, Vincerx CSO Hans-Georg is first author on a paper published in 2018 highlighting the use of KSP inhibitors in this context. He showed great data in an in vivo NSCLC xenograft model with a KSP-anti-TWEAKR ADC. One thing to note is that the KSP inhibitor being used in the antibodies Vincerx is taking forward is attached to a "Cell Trapper" sequence that reduces membrane permeability of the KSPi and limits its release from targeted cells after uptake. This could limit off-target effects and provide an improved safety profile over other ADCs which have been shown to cause myelosuppression, hepatotoxicity and peripheral neuropathy.
The KSPi toxophore has not been used by others as a payload in ADC constructs as far as I can see. Targeted delivery is going to be key to achieve higher doses at tumor site, to limit off-target toxicity as well as generate efficacious outcomes. This is going to be key for something like this, and I look forward to hearing more from Vincerx about these programs.
This is a stable linker specifically cleaved by the tumor-associated protease, legumain. The ADC is optimised to avoid payload de-conjugation except after cleavage by legumain. After endosomal cleavage, the KSP inhibitor is thought to be released into the intracellular compartment where it inhibits formation of kinesin spindles thereby impairing cellular functions, mitosis and inducing apoptosis.
VIP943 & VIP924 - Data
The company has said that no neutropenia, thrombocytopenia, liver toxicity or mucositis was observed with VIP943 in up to doses of 20 mg/kg (single dose) and 10 mg/kg (repeated dose) in monkey toxicology results. They have seen high efficacy in AML and NHL xenograft models.
Some pre-clinical work was presented at AACR 2019 on VIP924 (as BAY-924) (Abstract 4825) where high activity and specificity were seen in in vivo MCL (Myeloid cell leukemia) and ABC-DLBCL xenograft models.
Key Intellectual Property
As summarised below.
|Asset||Patent type||Earliest expiry||Jurisdiction|
|VIP236||COM||2039||Patent Cooperation Treaty|
|VIP943||COM||Dec 2037||Pending (US, EU, China, JPN, India, ARG, BR, MX)|
|VIP924||COM||2039||Patent Cooperation Treaty|
Bayer License Agreement
All of Vincerx's candidates were exclusively licensed from Bayer with a current agreement signed on October 7 2020. 5 M upfront was paid to Bayer upon Business Combination with Lifesci. The total milestones to be paid (if all achieved) range from 110 M to 318 M per licensed product. Tiered royalties to be paid to Bayer on worldwide net commercial sales are at rates from single digit to low double-digit percentages.
The company is currently advancing its Phase 1b study of VIP152 in MYC-driven r/r aggressive lymphomas and advanced solid tumors with another Phase 1b dose escalation study in CLL r/r to venetoclax and BTK inhibitors to initiate in 2H21. A Phase 2 combination study of VIP152 in combination with Pembrolizumab is also being planned to initiate in 2H22 for Myc abberated solid tumors. An IND filing for VIP236 is expected in the second half of 2022.
Disclosure: I am a shareholder of Vincerx Pharma as of the time of the publishing of this article. I may exit from this position at any given time without notice. Data presented in this article have been obtained from third-party publications and sources. I do not guarantee the accuracy of this data and all information presented here should be checked and verified accordingly. Readers of this article should each make their own evaluation and judgement of the mentioned companies and of the relevance and adequacy of the information provided. Readers should make other such investigation as deemed necessary. The article is intended for informational purposes. Investors and potential investors are requested to do additional research before investing in any of the companies mentioned in this article. All investments have risks of loss associated with them. Investing is very risky, highly speculative, and should not be done by anyone who cannot afford to lose the entire value of investment and without prior due diligence. Investors should evaluate the risks associated with each individual company before investing.
Additional disclosure: This article contains trademarks, trade names and copyrights of Vincerx and other companies, which are the property of their respective owners.
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