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Test Number : 156-115.80
Test Name : Check Point Certified Security Master - R80 (CCSM)
Vendor Name : Checkpoint
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156-115.80 test Format | 156-115.80 Course Contents | 156-115.80 Course Outline | 156-115.80 test Syllabus | 156-115.80 test Objectives

Exam ID : 156-115.80
Exam Title : Check Point Certified Security Master - R80
Questions : 100
Pass Marks : 70%
Duration : 90 minutes

- How policy changes impact chain module behavior
- Identify the source of UGI client connectivity problems
- Troubleshoot Secure Internal Communication issues
- Configure VPN Tunnel Interface
- Deploy IPv6 in a local environment
- Use commands to clear the connections table
- Configure Open Shortest Path First
- Troubleshoot NAT stages
- Identify connections in ClusterXL debug file

The Check Point Security Master course is designed for security experts who need to perform advanced deployment configurations of a Security Gateway and are working towards their Check Point Certified Cyber Security Master (CCSM) certification.

Our top technical certification proves the ability to perform advanced troubleshooting
CCSMs get Expert level access to SecureKnowledge
The CCSM is entitled to fast path access to Tier 3 Support
Their CCSMs belong to a small group of elite security professionals in the world

CCSM Objectives
Chapter 1 - Advanced Database Management
Obtain a deeper knowledge of the Security Management Architecture.
Understand how the Security Management Server uses key processes and debugs.
Review how objects are represented in the database.
Understand how GuiDBedit operates.
Do you know=>
What is Solr=>
Which ports are used for SIC=>
Which database does R80.x use for storing all objects=>
What is the syntax of a command for debugging issues with the internal Certificate Authority=>
Which process is responsible for the Management HA synchronization=>
Which command can be used to see the list of processes monitored by the Watch Dog process=>
Chapter 2 Kernel Mode and User Mode Troubleshooting
Understand how to use fw monitor to capture packets.
Understand how to use the fw debug process and debug infrastructures for User mode debugging.
Discuss how to enable and use core dumps when a User mode process crashes.
Do you know=>
When running a debug with fw monitor, which parameter will create a more verbose output=>
What is the proper command for allowing the system to create core files=>
Which command will clean the buffer and change all kernel debug properties to the default=>
What are benefits of the fw ctl zdebug command=>
Which directory are the usermode core files located in=>
What are some special considerations that should be taken into consideration while running fw monitor on production firewall=>
Chapter 3 - SmartConsole and Policy Management
Understand how to troubleshoot and debug SmartConsole issues.
Understand how to troubleshoot and debug issues that may occur during policy installation.
Do you know=>
Which process is first called when the policy installation command is initiated from the SmartConsole=>
Explain what the SCConfigManager.exe tool is used for and how to use it=>
What information is contained in a crash report from a SmartConsole application crash=>
Chapter 4 Advanced Network Address Translation
Understand how to troubleshoot and debug NAT issues using Gaia commands.
Understand Client Side and Server Side NAT.
Describe how to configure port mapping services.
Do you know=>
Which kernel debug flag should you use to troubleshoot NAT connections=>
What is the difference between Client-Side and Server-Side NAT=>
What table would you review to investigate a port exhaustion error when using Hide NAT=>
Chapter 5 - VPN Troubleshooting
Recognize how to debug VPN-related issues.
Do you know=>
Which Check Point utility should be used use to assist in analyzing the output of vpn and ike debug=>
What is the benefit of running vpn debug trunc over vpn debug on=>
Which command would you use in the process of deleting the IPSec Key to a specific given
Understand the infrastructure processes and components used for policy installation and processing packets in Access Control policies.
Understand how to troubleshoot and debug issues that may occur with Application Control and URL Filtering.
Understand how to debug HTTPS Inspection related issues.
Understand how to troubleshoot and debug Content Awareness issues.
Do you know=>
Which Daemon should be debugged for HTTPS Inspection related issues=>
Which daemon would you debug if you have issues with acquiring identities via identity sharing and sharing identities with other gateways=>
What does CMI stand for in relation to the Access Control Policy=>
Packet processing infrastructure consists of which components=>
Understand how to troubleshoot and debug issues that may occur with Threat Prevention Policies.
Understand how to troubleshoot Anti-Bot and Antivirus issues.
Discuss how to use IPS Bypass to manage performance issues.
Understand how to configure IPS to reduce false positives.
Do you know=>
Which process is enabled when the Policy Conversion process has the debug turned on using the INTERNAL_POLICY_LOADING=1 command=>
Which daemon is the main CLI process and daemon for Threat Extraction=>
How many layers are incorporated in IPS detection and what are they called=>
Which daemon is responsible for anti-spam=>
Which Threat Prevention daemon is the core Threat Emulation engine and responsible for emulation files and communications with Threat Cloud=>
What are some measures you can take to prevent IPS false positives=>
Chapter 8 Optimization and Tuning
Understand how the server hardware and operating system affects the performance of the Security Gateway.
Understand how to evaluate hardware configurations for optimal performance.
Discover additional tools to assist in monitoring CPU utilization.
Do you know=>
What is the command to check the number of CoreXL firewall instances=>
What is the default and maximum number of entries in the ARP Cache Table in a Check Point appliance=>
How long (in hours) does the CPSizeMe script run by default=>
Chapter 9 Advanced Clustering
Understand how to monitor cluster status and work with critical devices.
Recognize how to troubleshoot state synchronization.
Do you know=>
Which command would you use in order to test a ClusterXL failover=>
What ClusterXL mechanism is used to verify that the interfaces of other cluster members are UP and communicates the status of cluster members=>
What ClusterXL mechanism is used to verify that the interfaces of other cluster members are UP and communicates the status of cluster members=>
What does changing the cphaconf set_ccp parameter do=>
What command can the administrator run to view the status of the registered critical devices=>
What does changing the cphaconf set_ccp parameter do=>
Recognize how to use fwaccel and sim to enable and disable accelerated traffic.
Understand how to use fwaccel dbg and sim dbg commands.
Understand how to configure CoreXL to enhance Security Gateway performance.
Do you know=>
What mechanism can be used to confirm that important traffic such as control connections are not dropped when a Security Gateway is under high load=>
What table does the command "fwaccel conns" pull information from=>
Which command would show the synchronization statistics between cluster members=>
What is the command to view the SecureXL connection table=>
Which command would you use to check CoreXL instances for IPv6 traffic=>
What does SIM handle=>
Chapter 11 Deploying IPv6
Understand how to deploy IPv6 in a local environment
Do you know=>
How would an administrator view the routing table on the Security Gateway of production network where IPv6 is being used=>
What is the command to monitor IPv6 traffic in Expert mode=>
Which Check Point feature is not supported when running IPv6=>

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Antibody engineers seek greatest drug concentrated on TIGIT checkpoint | 156-115.80 Questions and Answers and PDF Dumps

four antibodies are already in trials to check efficacy towards the rising checkpoint molecule TIGIT, but debate swirls around the importance of Fc binding for drug action.

The race to develop a primary-in-type checkpoint-blocking drug is heating up, with new medical statistics and investor money all buttressing the conception of concentrated on the co-inhibitory molecule TIGIT (formally called T cellphone immunoreceptor with immunoglobulin and ITIM domains) alongside obstruction of the programmed mobile loss of life-1 (PD-1) pathway to deal with melanoma. The combination approach seems safe and beneficial against a number of strong tumor types, according to two contemporary clinical assembly reports describing patients handled with Genentech’s completely human IgG1 monoclonal antibody (mAb) tiragolumab, essentially the most advanced anti-TIGIT remedy, now in late-stage scientific construction.

With or devoid of Fc? Drug makers pursuing anti-TIGIT checkpoint inhibitors are undecided no matter if the Fc portion of an mAb (decrease neighborhood in image) is price preserving intact. credit score: Kenneth Eward / Science source

Others are conserving pace, though, with new funding to look at various their TIGIT-targeting antibody candidates. In July, for example, iTeos Therapeutics went public, netting $201 million — on exact of $one hundred twenty five million in deepest capital raised prior in the yr — which should still permit the business to enhance its human anti-TIGIT IgG1 mAb EOS-448 into part 2 trials. In June, Mereo BioPharma in a similar fashion completed a $70 million financing round to growth etigilimab, a humanized IgG1 anti-TIGIT mAb prior to now shown to aid stabilize tumor boom and produce a favorable immune profile in sufferers.

TIGIT is “poised to be the subsequent validated checkpoint,” says Dhan Chand, head of drug discovery at Agenus, which itself will soon launch first-in-human trials involving two diverse anti-TIGIT antibodies, one monoclonal and one bispecific. “in case you’re going to be during this container — similar to with anti–PD-1 — you should have [an anti-TIGIT drug] on your toolbox,” adds Terry Rosen, CEO of Arcus Biosciences, which entered right into a collaborative building pact with Gilead Sciences in may additionally 2020 based in big half round TIGIT-directed therapy. Rosen describes TIGIT-directed antibodies because the “competencies subsequent backbone therapy” in immuno-oncology.

but even with a dozen candidates now in scientific checking out (table 1), and a couple of others nearing the first-in-human stage, many questions stay about how exactly TIGIT blockade promotes antitumor immunity. Some scientists emphasize the value of TIGIT signaling in dialing down innate and adaptive immune responses by way of limiting the effector services of cytotoxic T cells and natural killer (NK) cells. Others aspect to the immunosuppressive action of TIGIT in enhancing the undertaking of regulatory T (Treg) cells or in curbing the release of proinflammatory cytokines from dendritic cells.

table 1 Anti-TIGIT antibody medicine in scientific development

And whichever mechanism predominates might massively affect the medical success of the numerous anti-TIGIT treatment options jockeying to attain the industry, as a result of ameliorations in the Fc binding means of every antibody candidate. “There’s so a great deal debate about this Fc” situation among investors and trade insiders alike, says Daina Graybosch, a research analyst at SVB Leerink who specializes in immuno-oncology drugs. “americans preserve talking about it.”

All anti-TIGIT mAbs in trials today have one key ordinary attribute: they reveal excessive ranges of target affinity and receptor occupancy. In principle, then, they may still each be capable of keep away from TIGIT from binding its ligand, CD155, which should still support eliminate the inhibitory signal that impedes T cells and NK cells from attacking cancers. Plus, because CD155 serves double responsibility as a ligand for the co-stimulatory molecule CD226 (also called DNAX accent molecule-1, or DNAM-1), TIGIT blockade should still release CD155 to have interaction its alternate receptor, thereby extra promoting usual tumor-directed immunity.

the place the mAb candidates notably fluctuate is of their Fc areas — and, as Hassane Zarour, a tumor immunologist on the school of Pittsburgh Hillman melanoma center, points out: “the way you Fc-engineer the antibody is extraordinarily vital.”

Many, including Genentech’s tiragolumab and Merck’s humanized mAb vibostolimab, employ a wild-category IgG1 isotype and thus hold TIGIT-directed antibody-based cellular cytotoxicity (ADCC), an immune manner that destroys antibody-coated goal cells. This might aid be sure the remedies do away with pesky Treg cells that categorical high tiers of TIGIT and compromise antitumor immunity. however the drugs might additionally dissipate sought-after cytotoxic cells within the method. and not desperate to take that risk, some organizations — most notably, Arcus and Bristol-Myers Squibb (BMS) — have opted to make use of mutated IgG1 tails with inactivated Fc areas. Others, comparable to Compugen and Astellas Pharma, developed their candidates on IgG4 backbones that offer handiest vulnerable Fc binding.

in the meantime, antibodies from Seattle Genetics and Agenus have been engineered with souped-up Fc exercise. The rationale for Fc enhancement — or, at a minimal, retaining Fc effector characteristic — stems from the incontrovertible fact that, as Chand puts it, “there’s more to Fc than simply ADCC.” in the case of antibodies targeting cytotoxic T-lymphocyte-linked protein 4 (CTLA-four) and TIGIT as a minimum, Chand’s crew at Agenus confirmed that intact Fc zones are essential to fuel interactions with dendritic cells, whose Fc-γ receptors (FcγRs) latch onto the antibodies and cause a kind of mobile reprogramming that enhances antigen-particular T cell responses, independent of any Treg mobile depletion. “if you happen to promote more desirable FcγR co-engagement, what you become doing is creating a glue between a T mobilephone and an antigen-providing phone — and that stabilization of the immune synapse results in a lot superior T cell activation,” explains Chand.

at the 2019 Society for Immunotherapy of cancer (SITC) annual meeting, a crew from Merck research Laboratories in Boston also said preclinical statistics showing that dendritic-telephone activation mediated by using FcγR co-engagement of an antibody to mouse TIGIT induces cytokine and chemokine expression, which in turn promotes immune infiltration into the tumor microenvironment and boosts co-stimulatory immune signaling. Mouse information from Genentech, iTeos and OncoMed prescribed drugs (which final year merged with Mereo) all extra imply that Fc binding is indispensable to the tumor-shrinking activity of anti-TIGIT treatment options. “Now, no matter if [Fc activity] will in reality endure out as a scientific differentiator I feel is still to be considered,” says Cathi Ahearn, vice chairman of global product strategy for Genentech’s oncology business unit.

The only obtainable phase 2 data come from a look at of patients with newly clinically determined non-small-cell lung melanoma (NSCLC) involving Genentech’s tiragolumab combined with the business’s Tecentriq (atezolizumab), an Fc-engineered, humanized, non-glycosylated IgG1κ mAb that objectives PD-1’s binding companion, PD-L1. As said on the 2020 American Society of clinical Oncology annual meeting in may additionally, the drug routine yielded a stronger response fee and extended development-free survival times compared to medication with atezolizumab on my own. Parsing the patients by using their tumors’ PD-L1 ranges, despite the fact, confirmed that the addition of tiragolumab was really helpful handiest when the immune regulatory molecule turned into expressed by means of at the least 50% of melanoma cells. In that cohort, tumor shrinkage came about essentially three times as regularly amongst patients who bought the mixture.

To ascertain that outcome, Genentech is now operating a registration-enabling trial involving 500 patients with previously untreated NSCLC and PD-L1–excessive tumors. a different part 3 trial is evaluating the identical combination of anti-TIGIT tiragolumab and anti–PD-L1 Tecentriq, in tandem with induction chemotherapy, in four hundred patients with huge small-cell lung cancer. Smaller trials concentrated on other tumor forms, including cervical cancer and multiple myeloma, are ongoing.

on the equal time, Merck is relocating forward with giant section 2 reports of its own anti-TIGIT candidate, vibostolimab, given in mixture with different brokers, including the PD-1 inhibitor Keytruda (pembrolizumab; a humanized IgG4κ mAb) to sufferers with advanced NSCLC or melanoma. The enterprise has already pronounced early information from the dose escalation element of a phase 1 solid tumor analyze; greater results from an extended cohort of sufferers with NSCLC are expected in September on the European Society for scientific Oncology virtual congress.

Taylor Schreiber, CEO of Shattuck Labs, is looking forward to discovering these consequences. If Merck’s vibostolimab works about as well as Genentech’s tiragolumab, he says, “you could as a minimum make the conclusion that effector competence isn't inhibiting the effect of targeting TIGIT — and that is the leading issue you’d be panic about.” Conversely, if Arcus’s humanized IgG1 mAb domvanalimab, with its Fc-disabled region, indicates close-equivalency to the different brokers, then it’s the TIGIT-blockading feature of those antibody therapies that doubtless concerns more than any Fc–FcγR co-engagement. preliminary part 1 records from the domvanalimab trial are anticipated at the next SITC assembly in November.

For his part, Schreiber remains debating no matter if to encompass an Fc-inactive IgG4 linker protein or an afucosylated IgG1 with greater Fc endeavor in Shattuck’s TIGIT-directed therapy, a bifunctional fusion protein now in preclinical toxicology testing. He plans to make a decision after seeing both the Merck and Arcus records. “That will be informative,” Schreiber says.

Rosen, the Arcus CEO, isn’t too panic about such comparisons, although. That’s as a result of his enterprise isn't focused on the identical method of dual checkpoint inhibition that others are pursuing. On properly of TIGIT and PD-1 blockade, Arcus is planning to take a 3-pronged attack on tumor immunosuppression with a small molecule drug designed to dam signaling of adenosine, an anti-inflammatory metabolite. “That’s going to be the vicinity where they bring improvement to sufferers and supply anything that provides to the box,” Rosen says. The business is now testing a triplet routine of its own experimental medicine: the TIGIT inhibitor domvanalimab, the PD-1 inhibitor wholly human IgG1 mAb zimberelimab and the small-molecule dual adenosine A2A/A2B receptor antagonist etrumadenant in sufferers with PD-L1-excessive NSCLC.

In a similar vein, iTeos is planning to evaluate its anti-TIGIT agent, EOS-448, together with its small-molecule A2A receptor antagonist EOS-850, plus or minus chemotherapy, within the coming 12 months. Likewise, Compugen is positioning its anti-TIGIT therapy, COM902, alongside the company’s inhibitor of poliovirus-receptor-linked immunoglobulin (PVRIG), a related co-inhibitory receptor that competes with DNAM-1 and TIGIT for binding to the CD122 ligand.

only by blockading both receptors, PVRIG and TIGIT, can “you truly liberate the arrest of the equipment and get enough immune stimulation,” says Compugen president and CEO Anat Cohen-Dayag. “more than that, there is an intersection between these two pathways and the PD-1 pathway,” she provides. “here's a triple pathway story and also you need the entire crucial pieces within the axis.” In part 1 trying out, Compugen’s anti-PVRIG drug, COM701, showed early indications of efficacy, each by itself and mixed with BMS’s PD-1 inhibitor Opdivo (nivolumab). Now, with COM902 nonetheless undergoing early clinical testing, Compugen has partnered with BMS to start evaluating the triple blockade strategy through the mixture of COM701, Opdivo and BMS-986207, one more anti-TIGIT drug that has already accomplished the safeguard component of a primary-in-human look at.

other businesses hope to carve out niches within the increasingly crowded anti-TIGIT area by way of trying out their experimental inhibitors in less commonplace tumor kinds, or through the use of TIGIT-pathway-selected biomarkers for patient choice. “We’re being very careful in precisely how they design these reviews,” says Mereo CEO Denise Scots-Knight. “We’re looking for white house right here.”

past melanoma, some academic agencies have also begun to consider instances wherein therapeutically augmenting TIGIT activity with an agonistic antibody may well be beneficial for sufferers. Nicole Joller, a T mobilephone immunologist at the college of Zurich in Switzerland, features to the illustration of extreme COVID-19 infections, in which many people journey extreme proinflammatory cytokine storms. “it's a surroundings where this could be helpful,” she says. “You may truly target TIGIT in anything else that’s marked with the aid of extreme inflammation, be it autoimmune or infection-mediated,” Joller notes.

Vijay Kuchroo, from Brigham and ladies’s sanatorium in Boston, says that he and fellow immunologist Dario Vignali, of the school of Pittsburgh school of medication, are now browsing across the idea of forming a company focused on advancing checkpoint agonists for treating autoimmunity. Few large drug companies seem to be pursuing this approach, youngsters Janssen scientists publicly offered in vitro information closing 12 months on the immunomodulatory effects of an agonist TIGIT-targeted human IgG1κ mAb referred to as TGTB227. based on spokesperson Kellie McLaughlin, the enterprise is “in the procedure of evaluating the potential of TGTB227 relative to different property in their portfolio.” She declined to comment on future construction plans.

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  • About this text Cite this text

    Dolgin, E. Antibody engineers are seeking for most appropriate drug focused on TIGIT checkpoint. Nat Biotechnol 38, 1007–1009 (2020).

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