1. Market Data
Fiscal Year June
Industry BioTech
Market Cap A$7.5M
Price/Earnings (ttm) N/A
Price/Book (mrq) 1.3x
Price/Sales (ttm) N/A
Top 20 Holder % 33%
Shares Outstanding 93.7M
Equity Float 80.6M
Avg. Volume (3 mo.) 230,497
As of March 29, 2016
Income Statement Snapshot
TTM
Revenue A$0.01M
Net Loss A($2.2M)
Balance Sheet Snapshot
MRQ
Cash A$1.9M
Debt A$0.0M
Company Website
prescienttherapeutics.com/
March 29, 2016
Target Price: A$0.46
Recent Price: A$0.08
Prescient
Therapeutics Ltd.
(ASX: PTX)
Company Overview
Prescient Therapeutics (“PTX,” “Prescient,” or the “Company”) is a clinical stage
oncology company developing novel compounds that show great promise as
potential new therapies to treat a range of cancers that have become resistant to
front-line chemotherapy. The Company’s novel compounds inhibit key tumor
survival pathways, restraining cancer growth across a variety of cancers including
breast, ovarian, leukemia, and multiple myeloma. PTX is currently in a Phase Ib/II
trial for breast cancer (partially funded by the U.S. Department of Defense), a Phase
Ib trial for ovarian cancer (partially funded by the National Cancer Institute), and
expects to initiate a Phase Ib trial for Acute Myeloid Leukemia (AML) in early
2016. The Company’s science/IP comes from Yale University and Moffitt Cancer
Center.
Valuation
Based on a NPV, we are valuing PTX at A$0.46. This values the Company’s five
clinical development programs for breast cancer (both PTX-200 and PTX-100),
ovarian cancer, AML, and multiple myeloma.
Investment Highlights
PTX’s therapies target the key tumor survival pathways Akt and Ras; Akt and
Ras activation is observed in a significant percentage of major cancer types
Drug resistance is one of the most significant problems in cancer therapy; PTX’s
therapies are designed to prevent or reverse resistance to cancer drugs
PTX has two cancer therapies in five different cancer clinical trials
Near-term data readouts during 2016 provide events that could lead to stock price
appreciation
Akt and Ras cause growth in cancer cells; PTX’s drug candidates block Akt and
Ras without generating off-target side effects
PTX-200 is currently in a Phase Ib/II trial for HER2- breast cancer; earlier trial
data showed anti-tumor activity and inhibition of tumor survival pathway Akt
PTX-200 is currently in a Phase Ib trial for ovarian cancer; current generic drugs
for ovarian cancer have low survival rates
PTX-200 is expected to enter a Phase Ib trial for AML in early 2016; earlier data
showed that over half of patients achieved stable disease after only one treatment
cycle, as well as reducing high p-Akt in AML patients blast cells
We believe that PTX-200 has shown the most impressive results from an Akt
inhibitor in AML to date
PTX-100 targets the Ras pathway; it is entering phase I for breast cancer and
multiple myeloma
Strong management team and key opinion leaders are backing PTX’s technology
2. Investment Highlights
PTX’s therapies target the key tumor survival pathways Akt and Ras; Akt and Ras activation is
observed in a significant percentage of major cancer types. PTX’s therapies are designed to target the
Akt and Ras biochemical “switches.” Preclinical data has shown that PTX’s therapies, when combined with
other established cancer drugs (this includes chemotherapy and biologics), inhibits cancer cell growth to a
greater degree than the cancer drug by itself. This indicates that PTX’s therapies may potentially be used as
either a stand-alone therapy or in combination with a wide variety of marketed oncology drugs. Akt and
Ras have generated significant interest from large pharmaceutical companies, due to the established basis
they have in contributing to the growth of a wide variety of major cancers. As the following chart shows,
Akt activation occurs at high percentages in a significant amount of major cancer types:
Tumor type % Tumors with active AKT
Glioma ~55
Thyroid carcinoma 80–100
Breast carcinoma 20–55
Small-cell lung carcinoma ~60
Non-small-cell lung carcinoma 30–75
Gastric carcinoma ~80
Gastrointestinal stromal tumors ~30
Pancreatic carcinoma 30–70
Bile duct carcinoma ~85
Ovarian carcinoma 40–70
Endometrial carcinoma >35
Prostate carcinoma 45–55
Renal cell carcinoma ~40
Anaplastic large-cell lymphoma 100
Acute myeloid leukemia ~70
Multiple myeloma ~90
Malignant mesothelioma
a
~65
Malignant melanomab
43–67
Ras activation has also been shown to occur in significant percentages in major cancers. Over 30% of all
human cancers are shown to have Ras mutations. PTX-100 targets geranylgeranyl transferase (GGTI),
which has been showed to greatly increase the risk of advanced cancer in breast cancer, endometrial
carcinoma, cervical cancer, prostate cancer, and liver cancer.
Targeted drugs such as PTX’s cancer therapies now make up the majority of the market for cancer
treatment, and the market share of targeted therapies is projected to continue to grow. Targeted therapies
have shown improved success rates in oncology clinical trials, as improved cancer testing and patient
screening have better identified which patients are likely to be responsive to a particular therapy. renal
cancer, and has shown anticancer activity against a variety of solid tumors. Next-generation mTOR
inhibitor everolimus is the standard of care for advanced pancreatic cancer, along with achieving approval
for a number of other cancers.
Drug resistance is one of the most significant problems in cancer therapy; PTX’s initial target
markets are focused on preventing or reversing resistance to cancer drugs. PTX’s drugs are designed
to prevent or reverse resistance to chemotherapy, which is one of the most significant problems in cancer
treatment. It is estimated that approximately 90% of metastatic cancers become resistant to chemotherapy.
Even targeted cancer treatments, such as HER-2 cancer drug Herceptin, develop resistance in the majority
a
Altomare et al. (2005)
b
Reviewed in Robertson (2005); remaining cancer types reviewed in Bellacosa et al. (2005)
Altomare, D., Testa J. Perturbations of the AKT signaling pathway in human cancer. Oncogene (2005) 24, 7455-
7464
3. of cases within one year of treatment for metastatic breast cancer (estimated to range from 66%-88%). The
following quote from University of Georgia associate professor Mandi Murph describes the importance of
overcoming chemotherapy resistance: “Within two years, 85 percent of women will have their (ovarian)
cancer come back in a more aggressive form … It is during that time that they won’t respond to the
chemotherapy … Chemoresistance prevents us from curing the disease … If we can cure chemoresistance,
we can cure ovarian cancer.” One of the most significant drivers of this resistance are the presence of
abnormal biochemical “switches” that, when turned on, contribute to cancer cell growth and lead to
metastasis.
PTX has two cancer therapies in five different cancer clinical trials. As the following chart shows, PTX
has two different cancer therapies that are currently engaged in five different human clinical trials:
PTX’s therapies have been the subject of over 65 peer reviewed publications to date. This indicates
enormous validation of the potential that the Company’s compounds have for treating cancer.
Near-term data readouts during 2016 provide events that could lead to stock price appreciation. The
PTX-200 clinical trials in breast cancer, ovarian cancer, and acute myeloid leukemia (AML) are scheduled
to have near-term data readouts during 2016. Positive data from these trials could lead to stock price
appreciation. The following table from the Company shows these near-term events:
4. Akt and Ras cause growth in cancer cells; PTX’s drug candidates block Akt and Ras without
generating off-target side effects. PTX-200 inhibits a tumor survival pathway known as Akt. Akt plays a
key role in the development of many cancers, including breast, ovarian, colorectal, prostate, pancreatic, and
hematological cancers. Given the wide range of cancers that Akt plays a role in, we believe that PTX-200
has significant platform potential over the long-term.
As the following diagrams show, PTX-200’s mechanism of action prevents Akt from anchoring to the cell
membrane, where it gets phosphorylated and activated, stimulating cancer cell division and growth:
5. PTX-100 has the ability to block an important cancer growth enzyme known as geranylgeranyl transferase
(GGT). This leads to the blocking/deactivation of the Ras tumor survival pathway. Mutations that directly
activate Ras are found in approximately 30% of cancers, and mutations occur more frequently in certain
types of cancers, including lung, colorectal, pancreatic, and melanoma. Previous treatments that attempted
to directly target Ras or target enzymes upstream of Ras have proven unsuccessful. PTX-100 is the first
drug in human clinical trials to attempt to block GGTI. The Ras signaling pathway is involved in many
other cancers through indirect activation. The Ras pathway is thought to play a role in approximately 50%
of breast cancers. Breast cancer is one of PTX-100’s current clinical trial programs.
PTX-200 is currently in a Phase Ib/II trial for HER2- breast cancer; earlier trial data showed anti-
tumor activity and inhibition of tumor survival pathway Akt. PTX-200 is currently in a phase Ib/II trial
for HER2- breast cancer. The trial combines PTX-200 with taxol in patients with metastatic and locally
advanced breast cancer. PTX’s Phase Ib/II trial in HER2- breast cancer is funded by a National Cancer
Institute (NCI) grant. All patients in the trial (n=17) have been dosed and the trial is now entering the
expansion phase. The recommended phase II dose of 35 mg/m2 has been determined.
The phase II portion of the trial is scheduled to commence during 1H16. The trial combines PTX-200 with
paclitaxel, followed by doxorubicin and cyclophosphamide. These milestones could provide important near
term news for PTX.
There are multiple Akt inhibitors in phase I and phase II trials for multiple different types of breast cancer,
as shown in the following chart:
Target Compound ClinicalTrial.gov identifier Setting
Akt inhibitors Perifosine NCT00054145 Phase II; MBC, completed
MK2206 NCT01245205 Phase I; MK-2206 with lapatinib in solid tumors with dose expansion in HER2+ breast cancer
NCT01281163 Phase Ib; MK-2206 with lapatinib in HER2+ MBC
NCT01277757 Phase II; MK2206 in advanced breast cancer with PIK3CA mutation, or AKT mutation, or PTEN loss/mutation
NCT01776008 Phase II; neoadjuvant MK-2206 with anastrozole with or without goserelin in stage 2 or 3 PIK3CA mutant HR+, HER2– breast cancer
GDC0068 NCT01562275 Phase Ib; GDC-0973 (MEK inhibitor) and GDC-0068 in solid tumors
Paplomata, E., O’Regan R. The PI3K/AKT/mTOR pathway in breast cancer: targets, trials and biomarkers. Ther Adv Med Oncol.
2014 Jul; 6(4): 154-166
Earlier trial data in HER2- breast cancer showed evidence of safety, anti-tumor activity, and inhibition of
important tumor survival pathway Akt. This indicates the potential for positive efficacy and safety data in
future clinical trials.
6. According to IMS Health, sales of breast cancer drugs are set to grow from $9.8 billion by 2013 to $18.2
billion by 2023, or a CAGR of 5.8%. The fastest growing market in breast cancer drugs is the HER2+
subtype, with this market set to grow from $5.6 billion in 2013 to $12.5 billion in 2013, or a CAGR of
7.6%.
HER2+ breast cancer accounts for approximately 20% of breast cancers; the outsized market growth is due
to the success of HER2+ breast cancer drugs such as Herceptin. PTX-200 is targeting HER2- breast cancer,
which encompasses the other 80% of breast cancers. In our view, the most promising breast cancer
category for PTX-200 is triple negative breast cancer, which makes up approximately 10-20% of breast
cancers. Most patients in this category have resistance to chemotherapy, and half of these patients die
within five years. Chemotherapy is the main treatment option to treat these patients.
Additionally, as the following table shows, the chemotherapy response rate in estrogen receptor (ER) and
hormone receptor (HR) positive advanced breast cancer, as defined by the pathological complete response
(pCR), is under 10%. Research indicates that activation of the Akt pathway increases resistance to
endocrine therapy. The pCR in ER- and HR-negative advanced breast cancer has been shown to range from
about 17%-33%.
First author n (% with positive ER/HR) pCR in ER/HR-positive (%) pCR in ER/HR-negative (%)
Bear 2286 (45) 8.2 16.7
Ring 435 (71) 8.1 21.6
von Minckwitz 904 (68) 6.2 22.8
Colleoni 399 (43) 7.6 33.3
Guarneri 1719 (67) 7.8 23.7
Barrios C., Sampaio C., Vinholes J., Caponero R. What is the role of chemotherapy in estrogen receptor-positive, advanced breast
cancer? Ann Oncol (2009) 20 (7): 1157-1162
Early-stage HER2- breast cancer shows better response rates to chemotherapy, but over half of patients still
show chemoresistance. Given the high rates of chemotherapy resistance in HER2- breast cancer, we believe
that a multibillion dollar market opportunity exists for PTX-200 in HER2- breast cancer.
PTX-200 is currently in a Phase Ib trial for ovarian cancer; current generic drugs for ovarian cancer
have low survival rates. PTX-200 is currently in a phase Ib/II trial for platinum-resistant ovarian cancer.
The trial combines PTX-200 with Carboplatin. The phase Ib trial is partially funded by the NCI.
A recent report from Visiongain projects that the ovarian cancer drug market will reach $1.7 billion by
2019, with growth driven mostly by the recent approvals of Yondelis and Avastin. Efficacy results from
these drugs were mediocre at best, with both drugs gaining EU approval but receiving rejection from the
FDA. Other ovarian cancer drugs currently in late-stage trials are projected to either not be approved or are
expected to have limited sales. Various targeted therapies in earlier-stage trials may provide improved
efficacy, although this is yet to be determined.
The primary treatment of ovarian cancer remains generic chemotherapies. Chemoresistance remains very
high, as indicated by high recurrence and mortality rates for ovarian cancer. Almost all patients who
receive chemotherapy for ovarian cancer are either resistant initially to chemotherapy or end up relapsing.
Prognosis following relapse is poor.
7. Big pharma has been testing Akt inhibitors in several early-stage clinical trials. Akt inhibitors are could
potentially show enhanced antitumor effects relative to mTOR inhibitors, as Akt acts upstream of mTOR.
The following table shows the Akt inhibitors that have published results in ovarian cancer:
Phase Treatment No. of OCpatients Selected toxicities Efficacy
I Perifosine (MTD = 150 mg/day) + docetaxel 21 Nausea, vomiting, anorexia, and fatigue
At MTD in 11 patients, PR in 1 PTEN-null patient, SD in 3
patients
I GSK795 (25, 50, or 75 mg/day) 12 Grade 2 anorexia (18%) and vomiting (18%)
2 (16%) cases of SD for 6 months with tumor shrinkage of
26% and 11%, respectively
I
GSK211 (50-150 mg/day) + carboplatin (AUC =
5) + paclitaxel (175 mg/m2)
29 Grade 1/2 diarrhea, nausea, and fatigue
All patients in dose escalation: ORR = 30%; At MTD: ORR =
50%
MTD, maximal tolerated dose; AUC, area under curve; SD, stable disease; ORR, objective response rate.
Cheaib B., Auguste A., Leary A. The PI3K/Akt/mTOR pathway in ovarian cancer: therapeutic opportunities and challenges. Chin J
Cancer. 2015 Jan; 34(1): 4-16
In addition to the compounds in the above table, there are a few other Akt inhibitors in clinical trials for
ovarian cancer. Below is a table detailing the current Akt inhibitors currently engaged in clinical trials:
Compound Trial Design Population Registration
MK - 2206 Phase II Monotherapy Recurrent Ovarian NCT01283035
AZD5363
Phase Ib plus olaparib
and AZD 2014 (mTOR
inhibitor) Phase I
monotherapy
Recurrent endometrial
and Ovarian Cancer
Advanced Malignancies
(Includes Ovarian)
NCT02208375
NCT01226516
GSK 2110183 Phase I/II dose finding
Platinum resistant
Ovarian Cancer
NCT01653912
Perifosine Phase I plus docetaxel
Relapsed Ovarian
Cancer
NCT00431054
Musa F., Schneider R. Targeting the PI3K/AKT/mTOR pathway in ovarian cancer. Transl Cancer Res 2015; 4(1): 97-106
PTX-200 is expected to enter a Phase Ib trial for AML in early 2016; earlier data showed that over
half of patients achieved stable disease after only one treatment cycle. PTX-200 is expected to enter a
phase Ib trial for AML in early 2016. The trial will combine PTX-200 with cytarabine in refractory or
relapsed acute leukemia.
A 32 patient phase I trial has been completed in AML. 17 out of 32 patients had achieved stable disease
after one treatment cycle, and three patients achieved a greater than 50% bone marrow blast reduction,
which is potentially indicative of PTX-200’s efficacy. PTX-200 also reduced pAKT in AML blasts,
providing another potential indicator of efficacy. PTX-200 was used as a monotherapy in its phase I trial,
and we think that efficacy has an opportunity to increase, given that it is now being combined with
cytarabine in its upcoming Phase Ib trial. Preclinical data showed that PTX-200 is highly synergistic with
cytarabine when treating AML cells:
8. PTX-200 was also shown to be safe, which is significant, given that past human trials in Akt inhibitors for
AML showed significant levels of toxicity.
AML survival rates are abysmal. For patients under 60 years old, the five-year survival rate is about 30%-
35%. For patients over 60 years old, the five-year survival rate is under 10%. As the patient population
ages, finding better treatment options for AML will be key. Primary chemotherapy treatment for AML
includes cytarabine. However, resistance typically occurs, as evidenced by the low AML survival rates.
We believe that PTX-200 has shown the most impressive results from an Akt inhibitor in AML to
date. In our view, the results from PTX-200 in AML are the most impressive results from an Akt inhibitor
in AML to date. As stated above, the Company’s phase I trial showed that 17 out of 32 patients achieved
stable disease after only one treatment cycle, and three patients achieved a greater than 50% bone marrow
blast reduction. Other published results in Akt inhibitors for AML have shown significant toxicity and low
overall response rates (ORR), as indicated in the below table of Akt inhibitors currently in clinical trials for
leukemia:
Compound Target Disease/ Model Result Reference
Perifosine AKT CLL phase II, ORR 1 (12,5%) of 8, SD 6 (75%) of 8 patients Friedman, Lanasa et al., Leuk Lymphoma, 2014 [134]
Perifosine + UCN-01 AKT AML phase I, ORR 0 (0%) of 11 patients Gojo, Perl et al., Invest New Drugs, 2013 [90]
GSK2141795 + MEK inhibitor AKT1/2/3 several cancer types in vitro efficacyin cell lines and murine models Dumble, Crouthamel et al., PLOS One, 2014 [135]
GSK2141795 + Trametinib AKT1/2/3 AML phase II, ongoing ClinicalTrials.govIdentifier: NCT01907815
MK-2206 AKT1 ALL Reversal of glucocorticoid resistance in vitro and in vivo Piovan, Yu et al., Cancer Cell, 2013 [52]
GSK690693 pan AKT ALL
in vitro inhibition of proliferation and induction of
apoptosis
Levy, Kahana et al., Blood, 2009 [136]
Fransecky L., Mochmann L., Baldus C. Outlook on PI3K/AKT/mTOR inhibition in acute leukemia. Mol Cell Ther. 2015; 3: 2.
PTX-100 targets the Ras pathway; it is entering phase I for breast cancer and multiple myeloma.
PTX-100 has been shown to be well tolerated in a study of advanced solid tumors. The trial had 13 patients
and determined a maximum tolerated dose of 2060 mg/kg. PTX-100 is set to enter phase I trials for breast
cancer and multiple myeloma, and the expected start dates for both trials are in 4Q16.
9. Preclinical results for PTX-100 (GGTI-2418) showed significant inhibitions in tumor growth volume. 100
mg/kg of PTX-100 daily resulted in a 94% reduction in tumor volume, and 200 mg/kg of PTX-100 every
third day resulted in a 77% reduction in tumor volume (p<0.005 for both treatment schedules).
There is a correlation between GGTI and both the overall risk of cancer and the probability of cancer to
grow and metastasize. GGTI blocks/deactivates the Ras pathway. Previous attempts to directly target Ras
have been unsuccessful, and clinical work is now either focusing on targeting upstream proteins that target
Ras (such as GGTI), or on pathways downstream of Ras. Until PTX-100, work focusing on targeting
upstream proteins of Ras has been confined to preclinical or very early clinical trial work (human clinical
trials targeting farnesyltransferase have been unsuccessful), while targets of downstream pathways of Ras
are in a variety of Phase I and Phase II clinical trials. PTX-100 is the only GGTI inhibitor in human clinical
trials.
PTX is planning to develop a novel cancer biomarker, p27, as a companion diagnostic to determine which
patients will respond best to PTX-100. It is thought that patients with low levels of p27 have overactive
Rho proteins. Rho proteins are part of the Ras pathway and are activated by GGTI (GGTI blocks the Ras
pathway and thus also blocks Rho proteins). P27 typically acts as a “brake” on cancer cell growth, and thus
low levels of p27 would likely lead to a greater risk of cancer cell growth. In one study of 167 node-
negative breast carcinomas 66% of women had low levels of p27. We believe that the development of p27
will increase the probability of successful trials for PTX.
Strong management team and key opinion leaders are backing PTX’s technology. PTX has amassed
an impressive management team, key opinion leaders, and clinical advocates to help run their upcoming
clinical trials in PTX-200. We believe that this helps in a number of ways, including assuring that company
resources are used in an effective manner, that PTX’s technology is of high quality and has strong
development potential, and that upcoming clinical trials will be run effectively and will be designed to best
assess the true efficacy and safety of PTX’s drugs.
Bios of key management, directors, and advisory personnel are available at the following links:
http://prescienttherapeutics.com/management-team/, http://prescienttherapeutics.com/directors/,
http://prescienttherapeutics.com/scientific-advisory-board/.
Patents granted in major jurisdictions until 2030. The Company’s patent portfolio should ensure that
PTX-200 and PTX-100, if they reach commercialization, will be able to sell their drugs on all major
revenue generating jurisdictions, and for a long enough period of time, to make development profitable and
worthwhile.
10. Valuation
Based on a rNPV, we are valuing PTX at A$0.46. This values the Company’s five clinical development
programs for breast cancer (both PTX-200 and PTX-100), ovarian cancer, AML, and multiple myeloma.
Some notes on our model:
- The majority of the Company’s value comes from PTX-200 in breast cancer and AML. We
believe that this is where the Company’s best clinical results have occurred to date. In particular,
we believe that PTX’s AML phase I trial results are the best results seen in an Akt inhibitor.
- We believe that the majority of the Company’s resources will be spent on developing PTX-200.
Our model assumes that partnering of the Company’s development programs occurs following
phase IIb results.
- We are assuming that the Company will raise an additional A$50 million at a weighted average
share price of A$0.25 to fund development of PTX-200 through phase IIb trials for breast cancer,
ovarian cancer, and AML, PTX-100 for breast cancer through a phase Ib/IIa trial, and PTX-100
for multiple myeloma through a phase Ia trial. We believe that the Company, if results are
positive, will be able to partner PTX-200 following phase IIb trials. Upfront license fees from
partnering can be used to fund other programs without further dilution.
- We are assuming that the Company’s per patient costs increase in its phase IIb trials for PTX-200.
This is assuming, in addition to the higher costs present with running a trial at additional centers,
that patients are screened for mutations that infer a higher probability of responding to an akt
inhibitor. This would increase trial costs, but also lead to a higher probability of trial success.
- Akt plays a role in a significant number of cancers, so we believe that the patient population that
would respond to an akt inhibitor could comprise a large percentage of the patient population.
- Given PTX-200’s positioning as an adjunctive therapy, strong safety profile, and strong
management team and client advocates, we believe that the Company will not have significant
issues with patient enrollment.
- We are assuming a per patient treatment price of A$47,000. We believe this is in line with the
prices of other small molecule kinase inhibitors.
- Our license, milestone, and royalty payments are based on licensing deals on a per indication
basis. If PTX were to execute a deal licensing PTX-200 for all indications, we believe that the fees
and royalties received would be much greater.
Ultimately, we think that PTX-200 could be prescribed as first- or second-line therapy in advanced stage
cancers. This is due to the need to prevent or reverse chemotherapy resistance as early as possible
(evidence suggests that chemoresistance rates increase following each failed therapy) and the fact that we
believe that it will be in the interest of chemotherapy marketers to combine PTX-200 with their
chemotherapy. This is because of the economic benefits that would be derived from using chemotherapy
treatment for a longer period of time.
11. Peer Comparison
Company Name Ticker
Share
Price
(USD)
Market Cap
(USD)
Cash
(MRQ, USD)
Total Debt
(MRQ, USD)
Rexahn Pharmaceuticals RNN 0.32 $69.2M $23.4M $0.0M
Sunesis Pharmaceuticals SNSS 0.54 $46.3M $26.9M $7.8M
MEI Pharma MEIP 1.20 $41.0M $53.8M $0.0M
Curis Inc CRIS 1.49 $192.2M $82.2M $24.2M
Verastem Inc VSTM 1.42 $52.5M $110.3M $0.0M
Median $52.5M $53.8M $0.0M
Average $80.3M $59.3M $6.4M
Prescient Therapeutics PTX.AX $0.06 $5.7M $1.4M $0.0M
Source: ThomsonReuters, as of March 29, 2016
The following table represents peer comparables that are developing kinase inhibitors. The closest
comparable, in our view, to PTX is RNN. RNN’s most advanced clinical trial program is an AKT-1
inhibitor in a phase IIa trial for metastatic renal cell carcinoma. CRIS’s lead compound is a HDAC and
PI3K inhibitor in a phase II trial for relapsed, refractory diffuse large B-cell lymphoma and a phase I trial in
patients with solid tumors. SNSS, MEIP, and VSTM experienced development setbacks throughout the
year and have all experienced 80%+ declines from their 52-week highs. The development setbacks for
SNSS and MEIP were in programs unrelated to kinase inhibitors. We believe that the strong valuations for
RNN and CRIS indicate the potential seen in kinase inhibitors, although all of the comps have a much
larger cash balance than PTX.
Risks
There is no guarantee that the Company’s clinical trials for PTX-200 or PTX-100 will show
statistically significant efficacy. There is no guarantee that the Company will achieve its primary
endpoints in its upcoming clinical trials. However, the Company has shown promising early data in breast
cancer, ovarian cancer, and AML for PTX-200.
PTX’s future capital needs are uncertain. While near-term capital needs are fairly certain, longer-term
capital needs are uncertain, and will be driven by such factors as clinical trial results, clinical trial design,
potential partnering with other pharma or biotech companies, and initiating clinical trials in new diseases.
Depending on how multiple factors occur, the Company’s capital raise needs could change significantly.
There is no guarantee that PTX-200 and PTX-100 will continue to show strong safety data. A portion
of kinase inhibitors have shown poor safety data in clinical trials. There is no guarantee that PTX-200 and
PTX-100 will continue to show strong safety data. Results to data have indicated that the Company’s drugs
are safe, and the unique mechanism of action of the drugs is thought to prevent the off-target effects seen in
other kinase inhibitors.
It is likely that the future commercial potential of PTX’s drugs will depend heavily on future
partnership agreements. We are currently modeling for PTX to partner their drugs following phase IIb
trials. Future potential cash flows from PTX’s drugs will depend heavily on the company or companies that
PTX partners with. This decision will likely impact phase III (or earlier if partnerships happen at an earlier
timepoint) trial designs, milestones/royalties received, and where and how effectively their drugs are
marketed if approved for commercial use.
13. Additional Information
Auditor: Ernst & Young
Company Information
Company Website
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Investor awareness services and programs are designed to help small-cap companies communicate their investment characteristics.
RedChip investor awareness services include the preparation of a research profile(s), multimedia marketing, and other awareness services.
Additional information about the subject security or RedChip Companies Inc. is available upon request. To learn more about RedChip’s
products and services, visit http://www.redchip.com/visibility/productsandservices.asp, call 1-800-RedChip (733-2447), or email
info@redchip.com.
Company Contact Info:
Prescient Therapeutics Ltd.
Level 4
100 Albert Road
South Melbourne VIC 3205
+61 3 9692 7222
justin@ptxtherapeutics.com
Investor Contact Info:
RedChip Companies, Inc.
1017 Maitland Center Commons Blvd.
Maitland, FL 32751
(407) 644-4256
www.redchip.com
