Accelerating Discoveries, Saving Lives
Scientists Demonstrate Long-Sought Drug Candidate Can Halt Tumor Growth
Researchers Identify Gene that Plays a Surprising Role in Combating Aging
Team Finds New Calorie-Burning Switch in Brown Fat
Professor Steven Reed: Cells and Stress
and more...
A Newsletter for Philanthropists Published Quarterly by The Scripps Research Institute
IN THIS ISSUE
3-5
RESEARCH UPDATES
Scientists Demonstrate Long-Sought Drug Candidate Can Halt Tumor Growth
Team Successfully Targets Common Mutation in ALS, Frontotemporal Dementia
Surprising Diversity of Antibody Family Provides Clues for HIV Vaccine Design
Researchers Link Alcohol-Dependence Gene to Neurotransmitter
Researchers Identify Gene that Plays a Surprising Role in Combating Aging
Team Finds New Calorie-Burning Switch in Brown Fat
Researchers Find Genetic Mutations Linked to Salivary Gland Tumors
TSRI Chemists Modify Antibiotic to Vanquish Resistant Bacteria
GIVING
5
6-9
A Gift that Makes a Difference to Medical Research
PROFILES
Donor Julie Hill: Shedding Light on the People of the World—and the Value of Medical Research
60 Seconds with TSRI Professor Steven Reed
10-11
APPOINTMENTS, AWARDS, HONORS
Peter Schultz Named Top Translational Researcher
Linda Sherman Assumes AAI Presidency
Team Awarded $4.4 Million to Investigate 10-Minute DNA Sequencing Technology
Karsten Sauer and Stephanie Rigaud Receive Immunology Award
Stephanie Sillivan Receives Early-Career Award
12
BACK COVER
TSRI Screening Center Helps Advance Drug Candidate to Clinical Trials
2
publisher: david blinder, senior vice president for external affairs
editors and contributing writers: elliot wolf and mika ono
illustration credit: cami abel photographers: john dole, james mcentee
RESEARCH UPDATES
Scripps Research Institute Scientists Demonstrate LongSought Drug Candidate Can Halt Tumor Growth
It’s a trick any cat burglar knows: to open a locked door, slide a credit card
past the latch.
Scientists at The Scripps Research Institute (TSRI) tried a similar strategy
when they attempted to disrupt the function of MYC, a cancer regulator
thought to be “undruggable.” The researchers found that a credit card-like
molecule they developed somehow moves in and disrupts the critical
interactions between MYC and its binding partner.
The research, published in the journal Proceedings of the National Academy of
Sciences, also shows the drug candidate can stop tumor growth in animal models.
“We finally hit a home run with this—maybe a grand slam,” said Kim Janda,
co-author of the new study and Ely R. Callaway, Jr. Professor of Chemistry,
director of the Worm Institute for Research and Medicine, and Skaggs
Scholar and member of the Skaggs Institute for Chemical Biology at TSRI.
Team Successfully Targets Common Mutation in
Lou Gehrig’s Disease, Frontotemporal Dementia
An international team led by scientists from TSRI’s Florida campus (Scripps
Florida) and the Mayo Clinic have for the first time successfully designed a
therapeutic strategy targeting a specific genetic mutation that causes a common
form of amyotrophic lateral sclerosis (ALS), better known as Lou Gehrig’s
disease, as well a type of frontotemporal dementia (FTD).
The scientists developed small-molecule drug candidates and showed they
interfere with the synthesis of an abnormal protein that plays a key role in
causing both diseases. The team also developed biomarkers that can test
the efficacy of this and other therapies.
The study, led by Professor Matthew Disney of TSRI and Professor of
Neuroscience Leonard Petrucelli of the Mayo Clinic, was published in the
journal Neuron.
“Our small molecules target a genetic defect that is by far the most major
cause of familial ALS, and if you have this defect you are assured of getting
ALS or FTD,” Disney said. “Our findings show for the first time that targeting
this mutation with a small-molecule drug candidate can inhibit toxic protein
translation—and establishes that it could be possible to treat a large number
of these patients, but this is just the start of these studies and additional
investigations need to be done.”
Currently, ALS is usually fatal two to five years after diagnosis, and there is
no effective treatment for FTD, a neurodegenerative disease that destroys
neurons in the frontal lobes of the brain.
3
Surprising Diversity of Antibody Family
Provides Clues for HIV Vaccine Design
neurotransmitter that lowers anxiety and increases feelings
of relaxation.
TSRI scientists have described how a single family of antibodies that broadly neutralizes different strains of HIV has
evolved remarkably diverse structures to attack a vulnerable
site on the virus.
The findings
provide clues
for the design of
a future HIV
vaccine.
“This novel and seminal study provides insights into the cellular
mechanisms of alcohol dependence,” said TSRI Associate
Professor Marisa Roberto, a co-author of the paper. “Importantly,
the study also offers a correlation between rodent and human data.”
“In a sense, this
antibody family
takes more than
one shot on goal
in order to hit
divergent forms
of HIV,” said
The findings provide clues for the design
Ian A. Wilson,
of a future HIV vaccine.
the Hansen
Professor of Structural Biology, chair of the Department of
Integrative Structural and Computational Biology and
member of the Skaggs Institute for Chemical Biology at TSRI.
“The findings give us new options for vaccine design,” added
TSRI Professor Dennis R. Burton, who directs the International AIDS Vaccine Initiative’s (IAVI) Neutralizing Antibody
Consortium and the National Institutes of Health-sponsored
Center for HIV/AIDS Vaccine Immunology and Immunogen
Discovery (CHAVI-ID) at TSRI.
The new research, reported in the journal Cell, is part of a
broad effort to “retro design” an effective HIV vaccine, based
on an understanding of rare, natural antibodies that effectively
hit HIV’s most vulnerable sites.
Researchers Link Alcohol-Dependence Gene to
Neurotransmitter
TSRI scientists have solved the mystery of why a specific
signaling pathway can be associated with alcohol dependence.
This signaling pathway is regulated by a gene, called neurofibromatosis type 1 (Nf1), which TSRI scientists found is
linked with excessive drinking in mice. The new research
shows Nf1 regulates gamma-aminobutyric acid (GABA), a
In addition to showing that Nf1 is key to the regulation of
the GABA, the research, which was published recently in the
journal Biological Psychiatry, shows that variations in the human
version of the Nf1 gene are linked to alcohol-dependence risk
and severity in patients.
Pietro Paolo Sanna, associate professor at TSRI and the study’s
senior author, was optimistic about the long-term clinical
implications of the work. “A better understanding of the
molecular processes involved in the transition to alcohol
dependence will foster novel strategies for prevention and
therapy,” he said.
Researchers Identify Gene that Plays a
Surprising Role in Combating Aging
It is something of an eternal question: Can we slow or even
reverse the aging process? Even though genetic manipulations
can, in fact, alter some cellular dynamics, little is known
about the mechanisms of the aging process in living organisms.
Now scientists from Scripps Florida have found in animal
models that a single gene plays a surprising role in aging
that can be detected early on in development, a discovery
that could point toward the possibility of one day using
therapeutics, even some commonly used ones, to manipulate
the aging process itself.
“We believe that a previously uncharacterized developmental
gene known as Spns1 may mediate the aging process,” said
Shuji Kishi, a TSRI assistant professor who led the study,
published recently by the journal PLOS Genetics. “Even a
partial loss of Spns1 function can speed aging.”
Using various genetic approaches to disturb Spns1 during the
embryonic and/or larval stages of zebrafish—which have
emerged as a powerful system to study diseases associated
with development and aging—the scientists were able to
produce some models with a shortened life span, others that
lived long lives.
Team Finds New Calorie-Burning Switch in
Brown Fat
Biologists at The Scripps Research Institute (TSRI) have
identified a signaling pathway that switches on a powerful
calorie-burning process in brown fat cells.
The study, which was reported recently in the Proceedings
of the National Academy of Sciences, sheds light on a process
known as “brown fat thermogenesis,” which is of great interest
to medical researchers because it naturally stimulates weight
loss and may also protect against diabetes.
“This finding offers new possibilities for the therapeutic activation
of brown fat thermogenesis,” said team leader Anastasia Kralli,
associate professor in TSRI’s Departments of Chemical Physiology
and Cell Biology.
Researchers Find Genetic Mutations Linked to
Salivary Gland Tumors
Research conducted at Scripps Florida has discovered links
between a set of genes known to promote tumor growth and
mucoepidermoid carcinoma, an oral cancer that affects the
salivary glands. The discovery could help physicians develop new
treatments that target the cancer’s underlying genetic causes.
The research, recently published by the Proceedings of the
National Academy of Sciences, shows that a pair of proteins
joined together by a genetic mutation—known as CRTC1/
MAML2 (C1/M2)—work with MYC, a protein commonly
associated with other cancers, to promote the oral cancer’s
growth and spread.
“This research provides new insights into the molecular
mechanisms of these malignances and points to a new
direction for potential therapies,” says TSRI biologist
Michael Conkright, who led the study.
TSRI Chemists Modify Antibiotic to Vanquish
Resistant Bacteria
TSRI scientists have devised a new antibiotic based on vancomycin that is powerfully effective against vancomycin-resistant
strains of MRSA and other disease-causing bacteria.
The new vancomycin analog appears to have not one but
two distinct mechanisms of anti-microbial action, against
which bacteria probably cannot evolve resistance quickly.
“This is the prototype of analogues that, once introduced,
will still be in clinical use a generation or maybe even two
generations from now,” said Dale L. Boger, the Richard and
Alice Cramer Professor of Chemistry at TSRI.
The report by Boger and members of his laboratory was published recently by the Journal of the American Chemical
Society 
GIVING
A Gift that Makes a Difference to Medical Research
Throughout the year, you have read in Scripps Discovers
about our research programs that tackle many dreaded
diseases including cancer, diabetes, Alzheimer’s, Ebola
and more. Now is your opportunity to help accelerate
our research efforts with a year-end charitable gift to
The Scripps Research Institute (TSRI). Simply visit our
website at www.supportscrippsresearch.org and click on
the Donate Now button.
If you’d like to learn more about other types of gifts to
benefit TSRI, visit our planned giving website, Discover
the Benefits of Giving Wisely at www.plannedgiving.
scripps.edu. There you will find a resource of ideas and
information on how to support our world-class research
through estate and charitable planning, including tips for
calculating your charitable gifts tax deduction and
inspirational stories about people like you who have
supported TSRI with charitable planning.
Of course, if you would like to contact us directly, we
would be happy to help you maximize your charitable
opportunities and reach your financial goals. For more
information, please contact Geoff Graham, director of
planned giving and estates, at (858) 784-9365 or
gcgraham@scripps.edu. In Florida, contact Irv Geffen,
director of major gifts and planned giving, at (561)
228-2017 or igeffen@scripps.edu.
When considering charitable gifts, you are urged to seek
the advice of your own financial and legal advisor(s)
about your specific situation. 
5
DONOR PROFILE
Julie Hill: Shedding Light on the
People of the World—and the Value
of Medical Research
Julie Hill is a happily footloose world traveler and author with a restless
love of adventure, but she has faced challenging times as well.
An Alexandrian Greek, Julie met her late husband, Arthur, an Australian,
when both were in graduate school in America. It was a golden marriage
of 43 years, she says. Work opportunities brought them to faraway places
with names that began to enter international consciousness only decades
later—Thailand, the Philippines, Western Samoa and Afghanistan. Arthur
represented the Ford Foundation and later on the United Nations Development Program, while Julie entered the corporate world of AT&T.
In 1986, Arthur had been diagnosed with a rare blood cancer known as
hairy cell leukemia. He was treated with alpha interferon, but his immune
system was compromised, and he lost so much weight he appeared skeletal.
He was not expected to live. He read an article in The New York Times
about TSRI’s development of 2-CdA (now marketed as Leustatin®) for
the disease. He came to La Jolla and became patient #66 in 2-CdA clinical
trials. A week later, his physician, Dr. Alan Saven at Scripps Health, told him
that “there was no more circulating hairy cell leukemia.” He remained
disease-free for almost 12 years until he passed away from other causes.
“I’m impressed with the
inspiring enthusiasm of the young
scientists I met at TSRI.”
julie hill
world traveler and author
“Sometimes it’s difficult to be a believer, but I’m a true believer in TSRI,”
said Julie, “I’m convinced of the value of its research—it saved my
husband’s life. I’m also impressed with the inspiring enthusiasm of the
young scientists I met at TSRI.”
In the ensuing years after Arthur’s treatment, he and Julie became
major donors to TSRI. She remains a contributor and has created a
bequest to benefit TSRI in hopes that her support will result in an
endowed chair for cancer research for a young scientist, leading to
development of more treatments like 2-CdA.
Julie has spent the past four decades exploring the planet and writing
about it. Fluent in five languages, she authored the book Promises to
Keep in 2003, after her husband’s death, followed a few years later by
her second book, The Silk Road Revisited: Markets, Merchants, and
Minarets. This year, she published her third book, Privileged Witness:
Journeys of Rediscovery, where she takes us in hand on her journeys
around 20 countries, from Asia to Africa. Although she has met many
foreign dignitaries, what’s really rewarding for her is the interaction
with the common people, be they tribesmen, children, or just ordinary
folks trying to make a living and carve a better life for their children.
6
“I’m a true believer in TSRI.
I’m convinced of the value of its research—
it saved my husband’s life.”
julie hill
When Arthur Hill developed
hairy cell leukemia, he was
treated with 2-CdA—a
drug developed at Scripps
that cleared all signs of
his disease.
“In my travels I have discerned a similarity
among people who bear the same universal
aspirations: all want their children to lead a
better life and have a better future than theirs; they all cry, laugh, eat, worry
and die,” said Julie. “We share so much, but still have to work at understanding one another. When I travel to India, I meet kids on the road.
What do I ask beyond “What is your name?” So I
have learned the names of India’s leading cricket
players—the better to open a conversation with
those boys who loiter on the temple steps.”
In the nine months of the year that she’s home, Julie
mentors graduate students at the UCSD Graduate
School of International Relations and Pacific
Studies. She enjoys sharing her wisdom with
these students of various nationalities. “They
have become my extended family,” she said.
Julie is scheduled to speak at a lunch with a
group of TSRI graduate students, offering
thoughtful insights based on her international
experience on leadership, women in the workplace, negotiation tactics and inter-industry
transferable skills.
By investing in young “up-and-coming” scientists,
Julie Hill is both providing a meaningful tribute
to her late husband, Arthur, and playing a
critical role as a true partner in medical
research. 
7
Tell us about your research and the diseases it impacts.
SCIENTIST PROFILE
60 Seconds with: TSRI Professor Steven Reed
We work on many diverse projects. One area of particular interest to us
is how certain proteins determine whether cells will survive stress. Many
diseases, such as diabetes and a host of neurodegenerative diseases, are
due to stress-related cell death. We have discovered a promising pathway
that we think can keep cells alive and force them to function. This discovery
could result in many devastating diseases being mitigated and in some
cases, cured.
Parkinson’s disease is devastating and unfortunately there is no cure or
even an effective treatment because the disease is not really understood.
A number of years ago, we made a significant discovery that could lead
to a new therapeutic strategy for Parkinson’s disease, Huntington’s
disease, ALS, and other neurodegenerative diseases. We focused on an
enzyme known as parkin, whose absence causes an early-onset form of
Parkinson’s disease. Precisely how the loss of this enzyme leads to the
deaths of neurons had been unclear. But we showed that parkin’s loss
sharply reduces the level of another protein that normally helps protect
neurons from stress and therefore keeps them alive. We have therefore
focused on pharmacological ways of keeping levels of this protein high.
“It’s exciting that my whole career is
now culminating in doing something
useful for society.”
professor steven reed
One application, in addition to neurological diseases such as Parkinson’s
disease, is stroke, where a portion of the brain is starved of both nutrients
and oxygen. Since nerve cells can’t live long under these conditions and
because they can’t be regenerated, intellectual and motor deficits typically
occur after a stroke. There is currently nothing on the market that can
save these cells when under so-called ischemic conditions, but we’re
working towards a potential drug that could keep neurons alive and
thereby greatly reduce brain damage. Our work has evolved from basic
research on cell cultures to developing lead compounds that we’re now
testing in animal models. Hopefully, these will be successful and we can
fast track these treatments to clinical trials for stroke and other diseases.
We also work on cancer and have discovered a basic mechanism that
can enable developing cancer cells to sustain abnormal growth. This
work will hopefully lead to the targeting of this mechanism with drugs
and diagnostic techniques. We were able to illuminate the roles of two
nearly identical proteins that were known to be overexpressed in many
cancers, but no one understood why. It now appears that the proteins’
overexpression enables cancerous growth by nullifying a natural defense
against uncontrolled cell division. We have discovered, however, that
this makes those specific cancer cells extremely vulnerable to a specific
novel chemotherapeutic strategy.
How did you get involved in science?
Ever since I was five years old, I’ve been a science nerd—nothing else
appealed to me as much as the idea of becoming a scientist. Well, except
I wanted to be a rock star for a while but that didn’t pan out.
8
What motivates you and what do you hope to accomplish?
I’ve always wanted to know what makes things tick and to try to understand living things at a very fundamental level. In science, my career
started by focusing on the basic mechanisms that control cell division. This
eventually led me to the research of diseases, especially cancer, since it is a
disease of cell division. Our work on stroke and neurodegenerative diseases
is a spin-off of our work in cancer, where we had identified an interesting
protein. Actually my wife, Sanna, who works with me, took the research
in a different direction and found that it had other functions relevant to
survival of cells in the brain. Today, my primary interest is in using basic
biological knowledge to develop new therapeutic approaches and ultimately
drugs to cure diseases. It’s exciting that my whole career is now culminating
in doing something useful for society beyond the theoretical. This certainly
wasn’t a given when I started out.
Why did you come to TSRI and what do you like about it?
I came here in 1986 because I had the freedom to do what I wanted here—I
was able to spend more time and energy on my research than elsewhere. I
like the idea of being able to do what interests me without many competing
obligations. I have no regrets. It’s been a great run for me at TSRI. I’ve
also been able to train many great graduate students and postdoctoral fellows
who have gone on to do wonderful things—I’m still good friends with
many of them. San Diego is a great place to do research. It has such a
vibrant research community—it’s one of the most intensive high-quality
research zones in the world.
Do you have a need for private philanthropy for your research?
Philanthropy helps accelerate discoveries
in disease research—research is getting
more and more expensive with the
cutting-edge technologies that are now
available to us. National Institutes of
Health funding is extremely hard to come
by these days. The NIH is funding a much
smaller percentage of grants than before.
As a result, we have a number of projects
to test compounds in animal models that
have not yet been funded. These projects
could move forward with philanthropy,
and as a result, might be propelled rapidly
into clinical trials. So, the financial impact
of philanthropy can be real with the NIH
funding vacuum, which is not liable to
change anytime soon. Therefore, supporting
TSRI is likely to have a big impact on basic
science and the therapeutics that will treat
and cure human diseases. 
9
APPOINTMENTS, AWARDS
and HONORS
,
Peter Schultz Named Top Translational Researcher
Peter Schultz, Scripps Family Chair Professor and member of the Skaggs
Institute for Chemical Biology at TSRI, was ranked the top translational
researcher in 2013, according to a study in the August 2014 issue of
Nature Biotechnology.
The ranking is based on total patents awarded to faculty members at
their current affiliations who were among corresponding authors on 200
papers highlighted in 2013 in the publication SciBX.
Schultz tops the study’s list of 20 scientists with 93 U.S. and European
patents. Schultz’s translational research activities at TSRI are centered on
regenerative medicine, cancer, autoimmune and orphan/neglected diseases,
previously in collaboration with the Genomics Institute of the Novartis
Research Foundation and more recently with the California Institute for
Biomedical Research, where he serves as director.
Linda Sherman Assumes AAI Presidency
TSRI Professor Linda Sherman has assumed the presidency of the
American Association of Immunologists (AAI), a 101-year-old international
organization of scientists dedicated to advancing the knowledge of
immunology and its related disciplines.
An active AAI member for more than 30 years, Sherman began her one-year
term July 1. The 7,600-member professional organization fosters the
exchange of information and ideas among investigators and addresses
the potential integration of immunologic principles into clinical practice.
AAI also publishes the Journal of Immunology.
Sherman’s TSRI lab studies autoimmunity and tumor immunity, in
particular examining how expression of proteins in normal tissues or tumor
cells alters recognition and responsiveness by T lymphocytes to antigens of
these proteins.
Team Awarded $4.4 Million to Investigate 10-Minute DNA
Sequencing Technology
TSRI scientists have been awarded a four-year $4.4 million grant from
the National Human Genome Research Institute to advance DNA
sequencing technologies.
“If we can inexpensively, rapidly and accurately sequence the whole
genome, cancer treatments could be different and monitoring someone
during the course of treatment would be different,” said Professor M.
Reza Ghadiri, who is principal investigator of the grant.
Ghadiri will develop “lab on a chip” technology, technically known as
protein nanopore arrays, working toward techniques that could be used by
physicians for DNA sequencing to better tailor care to the individual patient.
10
In nanopore-based DNA sequencing, single strands of DNA pass through
microscopic holes while the holes “read” the bases in the DNA sequence
by detecting changes in electrical conductance. Current technology takes
at least one week to sequence an entire genome, but Ghadiri hopes that
by creating an array with thousands—or even millions of nanopores—
the DNA-sequencing process could be completed in 10 minutes. Ghadiri
said developing a more efficient process would also help lower the cost
of sequencing and make it more practical for patients and their doctors.
Karsten Sauer and Stephanie Rigaud Receive Immunology
Award
TSRI Associate Professor Karsten Sauer and Stephanie Rigaud, research
associate in the Sauer lab, have received a Careers Immunology Fellowship
award from the American Association of Immunologists (AAI), a 101-yearold international organization of scientists dedicated to advancing the
knowledge of immunology and its related disciplines.
The supported project studies signal transduction mechanisms that
ensure the generation of a pathogen-reactive but self-tolerant T cell
repertoire. Defects in these mechanisms cause immune deficiencies and
autoimmune diseases such as rheumatoid arthritis or type 1 diabetes. By
elucidating the underlying mechanisms, the Sauer lab hopes to ultimately
develop improved therapies for these serious and unpreventable diseases.
Stephanie Sillivan Receives Early-Career Award
Stephanie Sillivan, research associate in the Miller lab, has received a
Young Investigator Award from the Brain & Behavior Research Foundation (formerly NARSAD), a nonprofit organization that promotes
scientific research targeted at understanding the causes of, and improving
treatments for, mental illness.
The two-year NARSAD grant supports promising young scientists conducting neurobiological research, enabling early-career researchers to garner
pilot data for innovative ideas prior to achieving proof-of-concept for
their work.
Sillivan’s research is directed at understanding the mechanisms that
support long-term memories, in particular traumatic or pathogenic
memories that persevere over an extended period of time. This work has
broad implications for neuropsychiatric disorders with a memory component, such as post-traumatic stress disorder, Alzheimer’s disease and
substance use disorder. 
11
“At TSRI, the unique advantages we have in
terms of scientific environment, colleagues and
facilities means our impact on human health can
be disproportionately large.”
—hugh rosen
TSRI SCREENING CENTER HELPS
ADVANCE DRUG CANDIDATE
TO CLINICAL TRIALS
The Molecular Screening Center at TSRI’s California campus
has played an essential role in advancing to clinical trials a
new compound to treat multiple myeloma, the second-most
common form of cancer of the blood.
with Professor Raymond Deshaies of the California Institute
of Technology, TSRI scientists screened an NIH network
library of small molecules (nearly 220,000 at that time) searching
for potential p97 inhibitors. They narrowed the field to the
top 50 candidates—cutting years off the research process.
The compound, CB-5083, is produced by Cleave Biosciences,
a biotechnology company headquartered in Burlingame,
California. CB-5083 is a first-in-class, oral inhibitor of
p97, a critical enzyme that controls various aspects of
protein homeostasis.
Under the auspices of a National Institutes of Health (NIH)
Molecular Libraries Screen Centers Network grant, spearheaded by TSRI Professor Hugh Rosen and in collaboration
The CB-5083 Phase I clinical trial will evaluate the
compound’s safety and efficacy in multiple myeloma
patients with relapsed/refractory or refractory disease who
have not responded to other forms of therapy. According to
the National Cancer Institute, an estimated 70,000 people
are living with multiple myeloma in the U.S., and approximately 24,050 new cases will be diagnosed this year. 
To learn more about supporting TSRI’s cutting-edge research, please contact:
Geoff C. Graham
(858) 784-9365 or (800) 788.4931
gcgraham@scripps.edu
Alex Bruner
(561) 228-2013
abruner@scripps.edu
CA: 10550 North Torrey Pines Road, TPC-2
La Jolla, CA 92037
FL: 130 Scripps Way, 4B2
Jupiter, FL 33458
www.supportscrippsresearch.org
The Scripps Research Institute is a 501(c)(3) not-for-profit organization, Tax ID# 33-0435954. A copy of the official registration (#CH17266)
and financial information may be obtained from the Division of Consumer Services by calling toll-free (800-435-7352) within the State of Florida.
Registration does not imply endorsement, approval, or recommendation by the State.