Small Business Administration and Coronavirus Assistance

With the COVID-19 outbreak sweeping the country, and over 75% of Americans currently under shelter-in place orders, small businesses face a prolonged period of economic uncertainty. To help these businesses survive the coming months, Congress included several relief measures in the Coronavirus Aid, Relief, and Economic Security Act (CARES) Act, passed on March 27. The CARES Act provides wide-ranging relief for small businesses affected by the crisis, including hundreds of billions of dollars of loans and grants designed to ensure businesses keep employees on their payrolls and have the necessary cash to weather the crisis. Below, we highlight these resources and which businesses stand to benefit:

Paycheck Protection Program
Most businesses with 500 or fewer employees can apply to receive loans from the Paycheck Protection Program, which is designed to prevent widespread layoffs by small businesses. Businesses receiving this assistance can receive up to $10 million loans from banks and lenders backed by the federal government. If all employees are kept on the payroll for the next eight weeks, the principle on the loans will be forgiven and businesses will only be on the hook for interest. One caveat is that small businesses where venture capital firms have more than 50% equity are disqualified from participation. Many startups could be left out of the program under these rules.

Economic Injury Disaster Loans and Loan Advance
For small businesses who need additional assistance staying afloat, Economic Injury Disaster Loans and Loan Advances are available. Businesses can receive loans up to $2 million and $100,000 in loan advances. The advance does not have to be repaid and can serve as a lifeline for businesses currently experiencing a loss of revenue. Generally, businesses must be smaller than 500 employees to qualify. Additional requirements and the application page can be found here.

SBA Debt Relief
The SBA’s Debt Relief program can provide relief for businesses with existing loans or seeking to take out new loans. Under the new Debt Relief program, the SBA will pay the interest and principle of current 7(a) loans for a period of six months and new 7(a) loans issued until September 27, 2020.  7(a) loans are the SBA’s primary existing lending program for small business and can be issued in amounts of up to $10 million.

SBA Express Bridge Loans
Lenders already receiving loans from the Express Bridge Pilot program can now receive up to $25,000 in additional loans with additional paperwork. These funds can be accessed with fast turnaround and used while businesses apply for additional relief.

More information can be found at:

Finding Emory Innovations to Build Your Company’s Product Pipeline

Emory has approximately 600 technologies available to license at any given time. In particular, Emory offers a variety of live science resources such as therapeutics, diagnostics, and research tools that are marketed by Emory OTT.  

However, finding new technologies available at a university can be time-consuming and potentially frustrating for startups and established companies alike. Below are simple ways to find and remain up-to-date with technologies coming from Emory University.

  1. Subscribe to TechFeed to receive email notifications about products: TechFeed is a notification system where users can sign up to receive emails about recently added technologies. It can be individually customized to get notifications based on what products you’re interested in and how frequently you want to be notified. 

  2. Use our Technology Listings page: To get an improved searching experience with more accurate results, use our Google-powered search option. Through this, you can find non-confidential summaries of available technologies. Alternatively, if you’re looking for something around a specific indication or topic, click on Keywords in our word cloud and Technology Categories to get a list of these technologies.

  3. Visit our Featured Innovations page: Using these articles, you can get more information about and see real-world applications of available technologies.

  4. Contact our knowledgeable Marketing Associate, Quentin Thomas: Reach out to Quentin via email to request a hand-picked selection of technologies related to your needs and areas of interest. Quentin also encourages interested parties to set up a face-to-face conversation with him so he can guide the path from there. 

  5. Subscribe to our RSS feed and follow us on Twitter @Emory OTT: By doing this, you can stay up-to-date with all of our new technologies as soon as they’re listed on the website.

Additionally, to find a one-stop shop to find technologies from Emory as well as universities worldwide, there are a number of third-party listing services available to search free of charge, including the Association of University Technology Managers (AUTM) Innovation Market (AIM).

Our goal as technology matchmakers is to simplify the process for industry colleagues to find our technologies. If you have any suggestions on how we can improve this process, please contact us.

What is Diabetic Nephropathy?

Diabetic nephropathy, or diabetic kidney disease, is a common condition associated with Type I or Type II diabetes. It is estimated that about 20-40% of diabetic patients develop some form of kidney disease. If undetected, diabetic nephropathy can be a debilitating and dangerous disease, which is why people with diagnosed diabetes have to be frequently monitored for kidney function.

The main role of the kidneys is to filter the blood and remove waste and harmful products, while maintaining proteins, water and other useful substances. More specifically, kidneys contain small blood vessels called glomeruli that are responsible for filtering a large volume of blood every day. There are two kidneys in the human body, working together in a complementary manner. However, if one kidney stops working, the glomeruli in the other kidney start filtering more blood to compensate for the loss of function. This is why people can live without issues if they have at least one functioning kidney.

In unregulated diabetes, blood sugar levels are elevated, which slowly damages the glomeruli. Furthermore, many diabetics also have high blood pressure, which also stresses kidney function over time. When glomeruli stop functioning properly, protein starts leaking in the urine and eventually harmful waste may stay in the bloodstream, causing severe problems.

Thankfully, diabetic nephropathy can be prevented in most cases by maintaining regulated blood sugar levels. However, even if a patient reaches the early stages of nephropathy, blood sugar regulation can slow down the progression of kidney disease. If left untreated, both kidneys may fail, in which case interventional treatments such as dialysis or even a kidney transplant may be necessary. Transplants can come from compatible organ donors that have fully functional kidneys and a compatible blood type to the recipient. Frequently, transplants come from living donors, which often are family members wanting to help their loved ones.

More resources on diabetic nephropathy

  1. National Institute of Diabetes and Digestive and Kidney Diseases.

  2. National Kidney Foundation.

  3. American Heart Association.–diabetes

— Vicky Kanta


Two important updates 

  1.  All staff in the Office of Technology Transfer are now working remotely, telecommuting. The office is still open for business and fully functional. Please reach out and we are ready to help. To find a complete staff listing go to our staff page on our website.

  2. Any new request for an Unfunded Research Contract should be sent to ott-mta [at] emory [dot] edu. Please fill out the appropriate questionnaire from our website to reduce processing time. The review of the agreement can not start until this information is submitted.

  3. Submitting a disclosure form can now be done on-line with our new tool called IdeaGate. Please go to the IdeaGate website to submit.

  4. The blog posts will slow down during this work from home period.

The Promise of CRISPR-Cas

Our bodies are made up of various cell groups that can do different things depending on the combinations of proteins they contain. Proteins can do wonderfully complex things, from acting as oxygen sensors to molecular motors. All of the information for making these proteins is stored in our DNA. The DNA consists of four molecules (commonly called by the letters A,T,G,C) put together in long strings of specific sequences. Each part of our DNA containing the information for creating a single protein is called a gene, thus our DNA holds the “genetic code” for all the proteins our body can make. The “letters” in our genes are converted to another type of molecular-letter-string called mRNA, which is then converted into protein.

Courtesy of Genetic Alliance UK

We get our DNA from our parents, and have a separate paternal and maternal copy of the entire human genetic code. However, sometimes you can inherit a gene that leads to disease — your DNA creates a slightly altered or dysfunctional protein that can affect certain processes going on in your body. For example, people with sickle cell disease have a gene for hemoglobin that is one “letter” different from the “normal” code. Hemoglobin is the protein inside your red blood cells that lets your body transport oxygen. When the code has been mutated through this one-letter change, it gives your red blood cells a sickle-like shape that can lead to many harmful effects.

Fixing a single base-pair mutation in our DNA could drastically change the shape of our blood cells, preventing sickle cell disease. Courtesy of Megan Hoban, UCLA.

Since many diseases are caused by very small alterations of our genetic code, it would be great if there was a way to change those codes carefully and correctly. While many methods have been designed to change the sequence of DNA, none of them are as easy to apply or as broadly effective as CRISPR-Cas, or simply CRISPR systems. CRISPR systems are groups of  proteins that are able to cut nucleic acids, like DNA, at specific points, when they have “guide RNAs” attached to them. To guide a CRISPR system to a pre-determined point in our DNA, we take advantage of the base pairing code. DNA is double stranded, and the letters A and G interact with the letters T and C on the other strand, respectively. Let’s say our target gene has an A at a specific position. Based on this complementary matching of letters, if we make our guide RNA have a T at the equivalent spot, it can interact with that A, too. Now if all the letters in our guide RNA are complementary to a certain gene sequence, the Cas protein will be chemically attracted toward that spot in your DNA. When it gets there, it will bind to the DNA, similarly to a Velcro strap, and make a precise cut. This way, we can make targeted small changes to specific genes causing known diseases, without causing any wide effects to the rest of the genetic code.

CRISPR interacting with DNA. Courtesy of Mirus Bio.

The ability to make site-specific cuts is an incredibly powerful tool in genetic engineering. Is there a protein you don’t want a cell to make? If you know the sequence of that protein, and therefore the sequence of its gene, you can cut it out. You can even add new genes by making a cut and putting something new in the middle — similar to ripping a piece of cloth apart and stitching a new fabric in the middle. With tools for genetic editing getting better every day, this is going to be a reality soon.

Even though CRISPR is a very powerful tool, there is plenty of debate in the scientific community about the rules that should govern its use in medicine. Since this method can be used to potentially eliminate diseases but also add features to organisms, important ethical issues have come up regarding use in animals and humans. The topic reached the news worldwide when a Chinese scientist, He Jiankui, announced that he used CRISPR to genetically modify two babies that were born through in vitro fertilization. The researcher had not received any official approval for these experiments and he was eventually fired from his position and is now facing prison time.

CRISPR ethics is still a fairly new field, but many government agencies like the National Institutes of Health have started working with bioethicists to study the best approach for regulating genetic editing. Since CRISPR is already widely used in research and even human clinical trials, scientists should always work in coordination with funding and governing agencies to continue exploring its benefits in an ethical and safe manner.  

— Devin Bog & Vicky Kanta

What are the Types of Kidney Failure?

Normal kidney function is fundamental for our health, since kidneys are tasked with removing waste from our bloodstream while keeping important nutrients. When kidneys stop performing this process, we are faced with a serious condition called kidney failure. Kidney failure is very prevalent worldwide, with approximately 5-10 million people dying every year from it. Since the human body has two kidneys, patients can survive if only one of the two is functioning. However, many times the conditions that damage our kidneys end up affecting both, which is why medical intervention is important.

There are two main categories of kidney failure: acute and chronic. The main difference has to do with the disease onset and progression rate. However, there may also be different underlying factors in their causes.

Acute kidney failure
In acute kidney failure (also called acute kidney injury), kidneys stop functioning over a very short period of time, usually a few days. There are many possible causes, but some of the most common ones have to do with decreased blood flow to the kidneys, direct injury to the kidneys or blockage of the urine pathway. Many times, acute kidney failure is a result of other conditions that bring patients to the hospital, which is why many times it occurs while patients are already hospitalized. Some examples are heart attacks, liver failure, or specific infections such as hemolytic uremic syndrome. Acute kidney failure is usually treated in the hospital with hemodialysis and dietary changes, until the kidneys restore their proper function.

Chronic kidney failure
In chronic kidney failure (or chronic kidney disease), the progression is slow and kidney function worsens over time. Some of the most prevalent causes are diabetes, hypertension and some genetic conditions that are associated with a family history of kidney failure. There are different stages of chronic kidney failure, measured by the ability of the kidneys to filter the blood. Based on the stage in which it is detected, chronic kidney failure can be treated with dietary changes and controlling the underlying condition. However, in late stages, special medication or hemodialysis may be required. If nothing else works, doctors may recommend a kidney transplant, which if successful may restore healthy kidney function.

Overall, kidney failure is treatable if detected early. Markers of deteriorating kidney function can be found in a simple blood test. This is why regular check-ups are important, especially if someone belongs to a group with a higher risk for developing kidney failure, such as diabetics, people with hypertension and older individuals.

More sources on kidney failure

  1. American Kidney Fund.

  2. National Institute of Diabetes and Digestive and Kidney Diseases.

  3. National Kidney Foundation.

— Vicky Kanta

What is a Pandemic?

Whenever a new disease emerges, the term “pandemic” is very commonly heard on the news and social media. However, its definition is not always clear. Briefly, a pandemic occurs when a new disease spreads widely across multiple areas of the world. There are some key characteristics that separate a pandemic from other epidemiological terms, such as endemics and epidemics; experts declare a pandemic when a) the infectious agent (e.g. a virus) causing the disease is entirely new or sufficiently different from existing ones, b) the number of cases in each area exceeds what is expected based on the population (i.e., an outbreak), and c) there are increased occurrences in various parts of the world simultaneously.

virus 3d illustrationThere have been various pandemics throughout history, such as the plague, the Spanish flu, etc. Although pandemics can be caused by any highly infectious agent, most recent instances are associated with novel strains of the influenza virus, which causes the flu. The influenza virus mutates constantly and is highly infectious, which is why many pandemics are caused by it. For example, the 2009 H1N1 pandemic was caused by a new strain of the Influenza A virus. This strain had many differences when compared to the seasonal flu strains, which were sufficient to render the existing flu vaccine mostly ineffective, and required the development of a specialized vaccine.

Nowadays, most countries have emergency preparedness plans for the possibility of future pandemics. However, there are also some simple things we can all do to limit the spread of disease and infection, such as washing our hands frequently, avoiding contact with sick individuals, and covering our cough and sneeze using the inside of our elbow.

More pandemic resources

  1. World Health Organization.

  2. Centers for Disease Control and Prevention.

  3. – Department of Homeland Security

— Vicky Kanta

How Does a Defibrillator Work?

Defibrillators are medical devices used to restore the heart’s regular rhythm. They work by delivering an electrical current or shock close to the heart to help the heart regain its normal beating pattern. There are different types of defibrillators that are either used in emergency settings or as a treatment to a chronic heart condition.

A common type of defibrillator is the Automated External Defibrillator or AED. This is a portable battery-powered device commonly found in public areas to be used in case of a medical emergency. In fact, many states have laws in place about the existence of AEDs in places such as schools, gyms, government buildings, etc. When someone shows signs of cardiac arrest, use of a defibrillator can help save the person’s life until medical personnel arrive. It has been estimated that quick use of an AED can increase chances of survival after cardiac arrest by 5-40%. AEDs come with detailed instructions so that even untrained individuals can assist with defibrillation. An AED will automatically analyze the person’s heartbeat pattern through sticky electrode pads applied on the chest and deliver a shock if deemed helpful.

Another type of defibrillator is the Implantable Cardioverter Defibrillator or ICD. ICDs are implanted under a person’s skin and track the heart rate. If an abnormality is detected, the ICD will deliver a shock at the right time, similarly to an AED. ICDs are used in patients with certain heart conditions who are at risk for dangerous heart rhythm abnormalities. Examples of such conditions are certain previous heart attacks, cardiomyopathies, and others.

More sources on defibrillators

  1. National Heart, Lung and Blood Institute.

  2. U.S. National Library of Medicine, MedlinePlus.

  3. American Heart Association.–treatment-of-arrhythmia/living-with-your-implantable-cardioverter-defibrillator-icd

  4. American Red Cross.

— Vicky Kanta

Faculty as Start-up Founder: One Man’s Experience

Raymond Dingledine, PhD is Emory professor of Pharmacology and co-founder of Emory’s screening facility. His research focuses on the pharmacology of glutamate receptors and the causes of epilepsy. Dingledine’s has received numerous awards such as the ASPET’s Robert R. Ruffolo Career Achievement Award in Pharmacology and election to the National Academy of Medicine. He has published over 200 research papers, served as editor of “Molecular Pharmacology,” and sat on the editorial board of “Molecular Interventions.” Ray is also co-founder of Emory start-up NeurOp. In this interview he shares some of his thoughts and experiences as co-founder of a company.

Raymond Dingledine, PhD

Tell me about your background/research interests. Were you always interested in research with commercial potential?

Raymond Dingledine, PhD is Emory professor of Pharmacology and co-founder of Emory’s screening facility. His research focuses on the pharmacology of glutamate receptors and the causes of epilepsy. Dingledine’s has received numerous awards such as the ASPET’s Robert R. Ruffolo Career Achievement Award in Pharmacology and election to the National Academy of Medicine. He has published over 200 research papers, served as editor of Molecular Pharmacology, and sat on the editorial board of Molecular Interventions. Ray is also co-founder of Emory start-up NeurOp. In this interview he shares some of his thoughts and experiences as co-founder of a company.

Tell me about your background/research interests. Were you always interested in research with commercial potential?

I became interested in the properties of glutamate receptors in the early 80’s. There were a number of amazing discoveries in the 80’s and 90’s that led to the gradual emergence of glutamate receptors as a major focus in neuroscience. One of the goals and recognitions early in this work was that NMDA receptor antagonists should be useful eventually as anti-ischemic compounds for cerebral ischemia, like stroke. The problem was that NMDA receptors play so many roles in the brain in daily activity that blocking them is simply not tolerated.

The field of pharmacology inherently has a therapeutic goal, so yes, I’ve always been interested in contributing to the long history of solving medical problems with new drugs. Stroke is a huge problem that has no solution right now other than try to dissolve the clot quickly. Steve Traynelis, another faculty member in Pharmacology, and I had been studying the molecular properties of NMDA receptors for quite a while. We discovered that there are some compounds that exert a pH-dependent block of NMDA receptors in such a way that the drugs are more potent at acidic pH. The idea is that you should be able to give a dose of an NMDA receptor blocker that does not affect NMDA receptors in healthy tissue. As soon as a stroke appears, oxygen is shut off to that part of the brain and you begin releasing lactate and other acidic metabolites, so there’s a local drop in pH. The idea is that our compounds would selectively target the penumbra of strokes that feature a low pH and that would solve the last problem in the long path of developing NMDA antagonists for clinical use.

Tell me a little about NeurOp. What do you market?

We don’t currently market anything. We formed the company in 2002 or 2003 to develop a first-in-class NMDA receptor antagonist. We now have developed a NMDA receptor antagonist internally that has just finished going through Phase I clinical trials with no unexpected toxicities, so we are at the point now of developing a Phase II trial.

When you formed NeurOp did you have the antagonist you wanted or was it something you had to produce?

Human Brain

When we formed NeurOp, we had nothing to license – what we had was a novel idea. The rationale for forming NeurOp, in hindsight, was basically a personal development. For about three years before NeurOp, I had considered several jobs at large pharma companies to essentially oversee the development of many NeurOp-like projects. I talked these opportunities over with a friend of mine named Sol Snyder from Johns Hopkins. He gave me pretty good advice, which was to keep my day job and accomplish my need to give back to society by forming one or more small purpose-built companies. So that’s what we did. Steve Traynelis, Jim McNamara (Duke) and I started NeurOp after that and I decided to stay at Emory in my academic roles.

What was your initial role in NeurOp? What is your role now?

Originally, I was a founder and member of the board of directors. I have the same role there today as a member of the board of directors. The difference is today, NeurOp is led by highly experienced former pharmaceutical executives and business-types. So, although in the early days I and the other founders had more of a decision-making role, now it’s a more traditional board of directors. I give advice to the CEO and he takes it or leaves it.

Steve Traynelis and I had a necessity to maintain a bit of an arm’s length with the goings on at NeurOp for conflict of interest reasons, so we were not involved directly in designing all of the pre-clinical studies. NeurOp was a fully functioning company with medicinal chemists, neuroscientists, clinical trialists, and clinicians. My role initially was as one of the decision makers, but now I’m more of an advisor to this company.

Was NeurOp your first venture into the world of startups? What expertise did you bring to the formation of this company?

NeurOp was my first startup. My business expertise at the time was limited to having served on advisory boards for companies like Merck, Lilly, Bristol Meyers, smaller companies. I’ve learned a lot along the way. At the beginning, we were such a small endeavor that everybody had to do everything, so there was no real distinction between the scientific and the business decisions. Today the business expertise is held by our leadership and other people on the board and my main contribution is on the scientific side.

How did you go about putting together the executive team of NeurOp? In what capacities had you worked with your current collaborators in the past?

The other two founders, Steve Traynelis and Jim McNamara from Duke, have been longtime scientific collaborators. I had worked with Jim since the late 70’s and Steve since the mid 80’s. We respect and complement one another’s expertise. Jim is a neurologist and Steve is a world class molecular pharmacologist. Dennis Liotta and Jim Snyder from Emory’s Chemistry department played major roles especially in the beginning in compound design.

We recruited a startup CEO, Vince La Terza who had previously been director of Emory’s OTT, so he knew his way around the local and southeast startup business communities. Then we got busy trying to raise money. It was extremely challenging. In the early days, we had nothing to license. We had an idea, we had some commercially available compounds, and a few that hadn’t been well characterized yet that were proprietary. We must have given 100 dog and pony shows to potential investors, both pharmaceutical company partners or venture capital angels.

We basically got two messages. One was “We like you boys, but you’re too early. Come back when you’ve been in man.” The second response was, “NMDA, oh my god.” The idea of the second one was that the pharmaceutical industry had already by that time spent more than a billion dollars in failed clinical trials for NMDA receptor antagonists and the general thought was that we shouldn’t be wasting our time on something that wouldn’t work. Most people were not really interested in the novel strategy of incorporating pH dependence to develop a conditional blocker, so it was very challenging.

We are right now trying to figure out what the best indication would be for a Phase II trial and we’re considering different stroke mechanisms or indications as well as pain and a couple of other ideas.

Has OTT been involved in the formation and success of your start up? If so, how?

In the early days, OTT was pretty passive, and I would say probably did not contribute very much. When Todd Sherer came along, the whole game shifted, and they are now the best they’ve ever been during my time at Emory. As NeurOp gained the ability to generate compounds on its own through its own medicinal chemists, the patents began shifting from Emory to NeurOp so for this effort, OTT didn’t contribute very much. Having said that, they were critical in licensing the compounds and they also helped us with the Georgia Research Alliance. GRA played a major role early on, eventually investing $450k.

What advice would you give a researcher interested in forming their own startup, based on the experience you’ve had with NeurOp?

We founded NeurOp too early when we basically only had an idea. We should have developed compounds internally at Emory and been closer to the point of having a clinical candidate before launching a company. I was influenced by my own need to get something going at the time and I should have held back on that. My advice would be to think carefully on the timing of the launch of a new company.

Three months ago, I cofounded a second company called Pyrefin to advance novel anti-inflammatory compounds through clinical trials. Our potential clinical indications are cognitive decline in epilepsy, endometriosis, arthritis, and potentially gliomas, all of which have been strongly benefitted by our compounds. The thing is, our science underpinning Pyrefin is about ten years ahead of where we were when we had founded NeurOp. Unless we run into unexpected toxicities or other problems during development, we’re done with basic discovery for the moment and we’ve selected clinical candidates and their backups.

Another piece of advice is something that was positive from both NeurOp and Pyrefin. Make sure that you are compatible with your cofounders. There will be inevitable questions about which direction to take, but if you respect one another and have an actual friendship, those conversations are so much easier to handle.

What is Atrial Fibrillation?

Atrial fibrillation (also called AFib) is a common condition in which the heart beats irregularly. More specifically, AFib occurs when the heart’s upper chambers (the atria) do not coordinate with the lower chambers (the ventricles) during a heartbeat. This results in an insufficient amount of blood being pumped from the atria to the ventricles, which subsequently leads to the rest of the body not receiving enough blood.

Patients with AFib report feeling heart palpitations or an irregular heartbeat. They may also feel faintness, fatigue or breathlessness, which may result from the inadequate blood flow to the body. AFib can be detected during a regular physical examination, through an electrocardiogram or a Holter monitor.

There are different types of AFib, depending on the frequency of the symptoms and their response to treatment. In paroxysmal AFib, symptoms go away within a week with or without treatment. In persistent AFib, symptoms are continuously present for at least a week and require treatment to recede. Finally, in permanent AFib, the rhythm cannot be restored to normal and long-term use of medication or other treatment is required.

AFib is usually treated by a combination of diet and lifestyle changes, along with medications such as beta blockers, calcium channel blockers or anticoagulants. For more severe cases, more invasive interventions may be required to help restore a normal heart rhythm. Some examples of such procedures are catheter ablation, which is minimally invasive, or surgical ablation, which is a full surgical procedure.

More sources on AFib

  1. National Heart, Lung and Blood Institute.

  2. Centers for Disease Control and Prevention.

  3. American Heart Association.

— Vicky Kanta